recombinant human tgf β1  (PeproTech)

 
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    Name:
    Recombinant Human TGF β1 CHO cell derived
    Description:
    The three mammalian isoforms of TGF β TGF β1 β2 β3 signal through the same receptor and elicit similar biological responses They are multifunctional cytokines that regulate cell proliferation growth differentiation and motility as well as synthesis and deposition of the extracellular matrix They are involved in various physiological processes including embryogenesis tissue remodeling and wound healing They are secreted predominantly as latent complexes which are stored at the cell surface and in the extracellular matrix The release of biologically active TGF β isoform from a latent complex involves proteolytic processing of the complex and or induction of conformational changes by proteins such as thrombospondin 1 TGF β1 is the most abundant isoform secreted by almost every cell type It was originally identified for its ability to induce phenotypic transformation of fibroblasts and recently it has been implicated in the formation of skin tumors Recombinant human TGF β1 is a 25 0 kDa protein composed of two identical 112 amino acid polypeptide chains linked by a single disulfide bond
    Catalog Number:
    100-21C-100UG
    Price:
    1,040.00
    Category:
    Recombinant Proteins
    Source:
    CHO cells
    Reactivity:
    Chicken Cow Dog Frog Monkey Mouse Pig Rabbit Rat
    Purity:
    98.0
    Quantity:
    100UG
    Buy from Supplier


    Structured Review

    PeproTech recombinant human tgf β1
    Autophagy inhibition rescued apoptosis in human peritoneal mesothelial cells. ( A and B ) Human peritoneal mesothelial cells pre‐treated with <t>TGF‐β1</t> (10 ng/ml) or transfected with siRNA Beclin1 were treated with 4.25% high‐glucose peritoneal dialysis solution (HGPDS) or vehicle for 24 hrs. The sum of early and late apoptotic cells ratio (%) was quantitated by flowcytometer analysis of Annexin V/PI. Results from three independent experiments are shown as means ± S.D. Results from three independent experiments are shown as means ± S.D. ** P
    The three mammalian isoforms of TGF β TGF β1 β2 β3 signal through the same receptor and elicit similar biological responses They are multifunctional cytokines that regulate cell proliferation growth differentiation and motility as well as synthesis and deposition of the extracellular matrix They are involved in various physiological processes including embryogenesis tissue remodeling and wound healing They are secreted predominantly as latent complexes which are stored at the cell surface and in the extracellular matrix The release of biologically active TGF β isoform from a latent complex involves proteolytic processing of the complex and or induction of conformational changes by proteins such as thrombospondin 1 TGF β1 is the most abundant isoform secreted by almost every cell type It was originally identified for its ability to induce phenotypic transformation of fibroblasts and recently it has been implicated in the formation of skin tumors Recombinant human TGF β1 is a 25 0 kDa protein composed of two identical 112 amino acid polypeptide chains linked by a single disulfide bond
    https://www.bioz.com/result/recombinant human tgf β1/product/PeproTech
    Average 99 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant human tgf β1 - by Bioz Stars, 2021-05
    99/100 stars

    Images

    1) Product Images from "Autophagy promotes fibrosis and apoptosis in the peritoneum during long‐term peritoneal dialysis"

    Article Title: Autophagy promotes fibrosis and apoptosis in the peritoneum during long‐term peritoneal dialysis

    Journal: Journal of Cellular and Molecular Medicine

    doi: 10.1111/jcmm.13393

    Autophagy inhibition rescued apoptosis in human peritoneal mesothelial cells. ( A and B ) Human peritoneal mesothelial cells pre‐treated with TGF‐β1 (10 ng/ml) or transfected with siRNA Beclin1 were treated with 4.25% high‐glucose peritoneal dialysis solution (HGPDS) or vehicle for 24 hrs. The sum of early and late apoptotic cells ratio (%) was quantitated by flowcytometer analysis of Annexin V/PI. Results from three independent experiments are shown as means ± S.D. Results from three independent experiments are shown as means ± S.D. ** P
    Figure Legend Snippet: Autophagy inhibition rescued apoptosis in human peritoneal mesothelial cells. ( A and B ) Human peritoneal mesothelial cells pre‐treated with TGF‐β1 (10 ng/ml) or transfected with siRNA Beclin1 were treated with 4.25% high‐glucose peritoneal dialysis solution (HGPDS) or vehicle for 24 hrs. The sum of early and late apoptotic cells ratio (%) was quantitated by flowcytometer analysis of Annexin V/PI. Results from three independent experiments are shown as means ± S.D. Results from three independent experiments are shown as means ± S.D. ** P

    Techniques Used: Inhibition, Transfection

    HPGDS induced Beclin 1‐dependent autophagy in human peritoneal mesothelial cells (HPMCs). ( A and B ) Transmission electron microscopy images of HPMCs following high‐glucose peritoneal dialysis solution (HGPDS) treatment. The HPMCs were treated with 4.25% HGPDS or vehicle for 24 hrs. Cells were then fixed immediately in 1% glutaraldehyde and post‐fixed in 2% osmium tetroxide. The cell pellets or sections were embedded in Epon resin. Representative areas were picked for ultrathin sectioning. Transmission electron microscopy is performed using a Tecnai G2 Spirit Bio TWIN (FEI Co.) at 120 kV. ( A ) The HPMCs were treated with vehicle as control (a) and 4.25% HGPDS for 24 hrs (b). Scale bars: 2 μm. ( B ) Cells treated with vehicle as a control with normal nuclear and organelles. N: nuclear; M: mitochondrion; ER: endoplasmic reticulum. Scale bars: 500 nm (a). Cells are treated with 4.25% HGPDS for 24 hrs. N: nuclear; White arrows, representative autophagic structures; Yellow arrows, degradative autophagic vacuoles. Scale bars: 1 μm (b, c and d), 500 nm (e and f). ( C ) Western blotting analysis shows the effect of 4.25% HPGDS treatment of cells transfected with siRNA Beclin 1 or siRNA Ctrl on MAP‐LC3 lipidation and p62/SQSTM1 expression. ( D ) Western blotting analysis shows the effect of 4.25% HPGDS treatment of cells cotreated with TGF‐β1 (10 ng/ml) on MAP‐LC3 lipidation and p62/SQSTM1 expression. ( E ) and ( F ) HPMCs pre‐treated with TGF‐β1 (10 ng/ml) or transfected with siRNA Beclin1 were treated with 4.25% HGPDS or vehicle for 24 hrs. Cells were then probed by SNLYSO sensor (an autolysosome florescent probe), and autophagic cells were analysed and quantitated by flowcytometer. Results from three independent experiments are shown as means ± S.D. ** P
    Figure Legend Snippet: HPGDS induced Beclin 1‐dependent autophagy in human peritoneal mesothelial cells (HPMCs). ( A and B ) Transmission electron microscopy images of HPMCs following high‐glucose peritoneal dialysis solution (HGPDS) treatment. The HPMCs were treated with 4.25% HGPDS or vehicle for 24 hrs. Cells were then fixed immediately in 1% glutaraldehyde and post‐fixed in 2% osmium tetroxide. The cell pellets or sections were embedded in Epon resin. Representative areas were picked for ultrathin sectioning. Transmission electron microscopy is performed using a Tecnai G2 Spirit Bio TWIN (FEI Co.) at 120 kV. ( A ) The HPMCs were treated with vehicle as control (a) and 4.25% HGPDS for 24 hrs (b). Scale bars: 2 μm. ( B ) Cells treated with vehicle as a control with normal nuclear and organelles. N: nuclear; M: mitochondrion; ER: endoplasmic reticulum. Scale bars: 500 nm (a). Cells are treated with 4.25% HGPDS for 24 hrs. N: nuclear; White arrows, representative autophagic structures; Yellow arrows, degradative autophagic vacuoles. Scale bars: 1 μm (b, c and d), 500 nm (e and f). ( C ) Western blotting analysis shows the effect of 4.25% HPGDS treatment of cells transfected with siRNA Beclin 1 or siRNA Ctrl on MAP‐LC3 lipidation and p62/SQSTM1 expression. ( D ) Western blotting analysis shows the effect of 4.25% HPGDS treatment of cells cotreated with TGF‐β1 (10 ng/ml) on MAP‐LC3 lipidation and p62/SQSTM1 expression. ( E ) and ( F ) HPMCs pre‐treated with TGF‐β1 (10 ng/ml) or transfected with siRNA Beclin1 were treated with 4.25% HGPDS or vehicle for 24 hrs. Cells were then probed by SNLYSO sensor (an autolysosome florescent probe), and autophagic cells were analysed and quantitated by flowcytometer. Results from three independent experiments are shown as means ± S.D. ** P

    Techniques Used: Transmission Assay, Electron Microscopy, Western Blot, Transfection, Expressing

    Expression of TGF‐β1, autophagy and EMT hallmarks in peritoneal membrane (PM) from patients before and with PD. ( A–D ) The PM tissues of each patient before and with PD were randomly selected for immunohistochemistry (IHC) assay. Representative photomicrographs of TGF‐β1, N‐cadherin, MAP‐LC3 and Beclin 1 expression as determined by IHC staining in peritoneum samples of patients before PD and with PD. Image magnification: 100× (left); 200× (right).
    Figure Legend Snippet: Expression of TGF‐β1, autophagy and EMT hallmarks in peritoneal membrane (PM) from patients before and with PD. ( A–D ) The PM tissues of each patient before and with PD were randomly selected for immunohistochemistry (IHC) assay. Representative photomicrographs of TGF‐β1, N‐cadherin, MAP‐LC3 and Beclin 1 expression as determined by IHC staining in peritoneum samples of patients before PD and with PD. Image magnification: 100× (left); 200× (right).

    Techniques Used: Expressing, Immunohistochemistry, Staining

    High‐glucose peritoneal dialysis solution (HGPDS) increased TGF‐β1 production, activated TGF‐β1/Smad2/3 signalling and induced autophagy, fibrosis and apoptosis hallmarks in human peritoneal mesothelial cells (HPMCs). ( A ) The levels of TGF‐β1 from Control, 1.5%, 2.5% and 4.25% HGPDS‐treated cells were determined by ELISA. Each bar represents the mean ± S.D. Statistical analysis was performed using Student's t ‐test, * P
    Figure Legend Snippet: High‐glucose peritoneal dialysis solution (HGPDS) increased TGF‐β1 production, activated TGF‐β1/Smad2/3 signalling and induced autophagy, fibrosis and apoptosis hallmarks in human peritoneal mesothelial cells (HPMCs). ( A ) The levels of TGF‐β1 from Control, 1.5%, 2.5% and 4.25% HGPDS‐treated cells were determined by ELISA. Each bar represents the mean ± S.D. Statistical analysis was performed using Student's t ‐test, * P

    Techniques Used: Enzyme-linked Immunosorbent Assay

    2) Product Images from "Differential Role of PTEN in Transforming Growth Factor β (TGF-β) Effects on Proliferation and Migration in Prostate Cancer Cells"

    Article Title: Differential Role of PTEN in Transforming Growth Factor β (TGF-β) Effects on Proliferation and Migration in Prostate Cancer Cells

    Journal: The Prostate

    doi: 10.1002/pros.23482

    PTEN is required for inhibitory effects of TGF-β on cell proliferation in DU145 cells ( A ) DU145 cells were treated with TGF-β1 or TGF-β3 (5ng/ml) to determine cell proliferation. Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: PTEN is required for inhibitory effects of TGF-β on cell proliferation in DU145 cells ( A ) DU145 cells were treated with TGF-β1 or TGF-β3 (5ng/ml) to determine cell proliferation. Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used:

    Endogenous PTEN inhibits effects ofTGF-β on cell migration in prostate cancer cells ( A ) DU145 cells transfected with control siRNA or PTEN siRNA were treated with TGF-β1 or TGF-β3 (5ng/ml), or EGF (10ng/ml) to determine migratory properties in a transwell cell migration assay. Levels of PTEN proteins after transfection with control siRNA or PTEN siRNA in DU145 cells were determined by western blotting analysis (inset). Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: Endogenous PTEN inhibits effects ofTGF-β on cell migration in prostate cancer cells ( A ) DU145 cells transfected with control siRNA or PTEN siRNA were treated with TGF-β1 or TGF-β3 (5ng/ml), or EGF (10ng/ml) to determine migratory properties in a transwell cell migration assay. Levels of PTEN proteins after transfection with control siRNA or PTEN siRNA in DU145 cells were determined by western blotting analysis (inset). Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used: Migration, Transfection, Cell Migration Assay, Western Blot

    TGF-β isoforms do not induce invasive behavior in DU145 cells Invasive properties of DU145 cells treated with TGF-β1 (5ng/ml), TGF-β3 (5ng/ml), or EGF (10ng/ml) were determined by an invasion assay. Cells were allowed to invade through a Matrigel coated porous membrane for 48 hours. Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: TGF-β isoforms do not induce invasive behavior in DU145 cells Invasive properties of DU145 cells treated with TGF-β1 (5ng/ml), TGF-β3 (5ng/ml), or EGF (10ng/ml) were determined by an invasion assay. Cells were allowed to invade through a Matrigel coated porous membrane for 48 hours. Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used: Invasion Assay

    TGF-β isoforms increase PTEN protein levels in DU145 and RWPE1 cells ( A ) RT-PCR analysis of PTEN gene expression in DU145 cells after treatment with TGF-β3 (5ng/ml) at specific time points and different doses of exogenous TGF-β3 for 4 hours. L-19 was used as a loading control. No reverse transcriptase (RT) samples derived from the same RNAs were also included. ( B ) Western blot analysis of PTEN protein levels in RWPE1 (upper panel) and DU145 (lower panel) cells after treatment for specific time periods with exogenous TGF-β1 and TGF-β3 (5ng/ml). Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: TGF-β isoforms increase PTEN protein levels in DU145 and RWPE1 cells ( A ) RT-PCR analysis of PTEN gene expression in DU145 cells after treatment with TGF-β3 (5ng/ml) at specific time points and different doses of exogenous TGF-β3 for 4 hours. L-19 was used as a loading control. No reverse transcriptase (RT) samples derived from the same RNAs were also included. ( B ) Western blot analysis of PTEN protein levels in RWPE1 (upper panel) and DU145 (lower panel) cells after treatment for specific time periods with exogenous TGF-β1 and TGF-β3 (5ng/ml). Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used: Reverse Transcription Polymerase Chain Reaction, Expressing, Derivative Assay, Western Blot

    TGF-β induces phosphorylation of Smad proteins in DU145 and RWPE1 cells (Western blot analyses of phosphorylated Smad2 (pSmad2) and Smad3 (pSmad3) in ( A ) DU145 cells and ( B ) RWPE1 cells after treatment with TGF-β1 or TGF-β3 (5ng/ml) for 15 and 30 minutes. Total Smad (Smad2/3) and β-actin were used as loading controls. Each bar represents mean ± SEM (n=3). Different letters denote significant differences among various groups ( P
    Figure Legend Snippet: TGF-β induces phosphorylation of Smad proteins in DU145 and RWPE1 cells (Western blot analyses of phosphorylated Smad2 (pSmad2) and Smad3 (pSmad3) in ( A ) DU145 cells and ( B ) RWPE1 cells after treatment with TGF-β1 or TGF-β3 (5ng/ml) for 15 and 30 minutes. Total Smad (Smad2/3) and β-actin were used as loading controls. Each bar represents mean ± SEM (n=3). Different letters denote significant differences among various groups ( P

    Techniques Used: Western Blot

    TGF-β isoforms have no synergistic or additive effect on cell proliferation and cell migration in different cell types ( A ) DU145 cells were treated with TGF-β1 or TGF-β3 (5ng/ml) or combined (TGF-β1 and TGF-β3) to determine cell proliferation. Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: TGF-β isoforms have no synergistic or additive effect on cell proliferation and cell migration in different cell types ( A ) DU145 cells were treated with TGF-β1 or TGF-β3 (5ng/ml) or combined (TGF-β1 and TGF-β3) to determine cell proliferation. Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used: Migration

    TGF-β isoforms exert differential effects on migratory properties in different prostate cancer cells ( A–C ) Cell migration of DU145, PC3, and LNCaP cells across transwell membranes were assayed in response to TGF-β1 (5ng/ml), TGF-β3 (5ng/ml), or EGF (10ng/ml) treatments. EGF was used as a positive control. Each bar represents mean ± SEM (n=3). *Significantly different ( P
    Figure Legend Snippet: TGF-β isoforms exert differential effects on migratory properties in different prostate cancer cells ( A–C ) Cell migration of DU145, PC3, and LNCaP cells across transwell membranes were assayed in response to TGF-β1 (5ng/ml), TGF-β3 (5ng/ml), or EGF (10ng/ml) treatments. EGF was used as a positive control. Each bar represents mean ± SEM (n=3). *Significantly different ( P

    Techniques Used: Migration, Positive Control

    3) Product Images from "Transforming growth factor-?1 Suppression of Endotoxin-induced Heme Oxygenase-1 in Macrophages Involves Activation of Smad2 and Downregulation of Ets-2"

    Article Title: Transforming growth factor-?1 Suppression of Endotoxin-induced Heme Oxygenase-1 in Macrophages Involves Activation of Smad2 and Downregulation of Ets-2

    Journal: Journal of cellular physiology

    doi: 10.1002/jcp.22741

    Smad2 is critical for TGF-β1 suppression of HO-1 during LPS exposure. (A) HO-1 promoter construct (−295/+74, 250 ng/well) was co-transfected into RAW 264.7 cells with a control plasmid, or with an expression plasmid for WT Smad2 (200 ng/well,
    Figure Legend Snippet: Smad2 is critical for TGF-β1 suppression of HO-1 during LPS exposure. (A) HO-1 promoter construct (−295/+74, 250 ng/well) was co-transfected into RAW 264.7 cells with a control plasmid, or with an expression plasmid for WT Smad2 (200 ng/well,

    Techniques Used: Construct, Transfection, Plasmid Preparation, Expressing

    TGF-β1 suppression of LPS-induced HO-1 gene expression. The schema illustrates the effect of TGF-β1 on LPS-induced HO-1. HO-1 is transcriptionally induced by LPS in macrophages, and this occurs in part by an increase in Ets-2 expression
    Figure Legend Snippet: TGF-β1 suppression of LPS-induced HO-1 gene expression. The schema illustrates the effect of TGF-β1 on LPS-induced HO-1. HO-1 is transcriptionally induced by LPS in macrophages, and this occurs in part by an increase in Ets-2 expression

    Techniques Used: Expressing

    EBS2 site is critical for the suppression of HO-1 promoter activity by TGF-β1. (A) Deletion constructs of the HO-1 promoter (−295/+74, −137/+74, −117/+74, and −66/+74) were transfected (250 ng/well) in RAW 264.7
    Figure Legend Snippet: EBS2 site is critical for the suppression of HO-1 promoter activity by TGF-β1. (A) Deletion constructs of the HO-1 promoter (−295/+74, −137/+74, −117/+74, and −66/+74) were transfected (250 ng/well) in RAW 264.7

    Techniques Used: Activity Assay, Construct, Transfection

    TGF-β1 suppresses LPS-induced HO-1 expression. Total RNA and protein were extracted from RAW 264.7 cells after TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1 administration at various time points. The expression of HO-1 mRNA
    Figure Legend Snippet: TGF-β1 suppresses LPS-induced HO-1 expression. Total RNA and protein were extracted from RAW 264.7 cells after TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1 administration at various time points. The expression of HO-1 mRNA

    Techniques Used: Expressing

    TGF-βRI inhibitor, SB431542, blocks the downregulation of HO-1 by TGF-β1. Total RNA and protein were extracted from RAW 264.7 cells 3 hours and 24 hours after administration of TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1,
    Figure Legend Snippet: TGF-βRI inhibitor, SB431542, blocks the downregulation of HO-1 by TGF-β1. Total RNA and protein were extracted from RAW 264.7 cells 3 hours and 24 hours after administration of TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1,

    Techniques Used:

    Effect of TGF-β1 on expression of signaling molecules during LPS exposure. RAW 264.7 cells were stimulated with TGF-β1 (10 ng/ml), LPS (10 ng/ml), or a combination of LPS+TGF-β1. Cell lysates were analyzed by Western blot for phosphorylated
    Figure Legend Snippet: Effect of TGF-β1 on expression of signaling molecules during LPS exposure. RAW 264.7 cells were stimulated with TGF-β1 (10 ng/ml), LPS (10 ng/ml), or a combination of LPS+TGF-β1. Cell lysates were analyzed by Western blot for phosphorylated

    Techniques Used: Expressing, Western Blot

    Effect of TGF-βRI inhibitor on TGF-β1 signaling during LPS exposure. Cells were treated with the TGF-βRI inhibitor (SB431542, 10 μM) for 30 minutes before TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1
    Figure Legend Snippet: Effect of TGF-βRI inhibitor on TGF-β1 signaling during LPS exposure. Cells were treated with the TGF-βRI inhibitor (SB431542, 10 μM) for 30 minutes before TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1

    Techniques Used:

    TGF-β1 downregulates the HO-1 transactivator, Ets-2, during LPS exposure. Total RNA and protein were extracted from RAW 264.7 cells after TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1 exposure at various time points (as depicted).
    Figure Legend Snippet: TGF-β1 downregulates the HO-1 transactivator, Ets-2, during LPS exposure. Total RNA and protein were extracted from RAW 264.7 cells after TGF-β1 (10 ng/ml), LPS (10 ng/ml), or LPS+TGF-β1 exposure at various time points (as depicted).

    Techniques Used:

    TGF-β1 suppresses HO-1 promoter activity during LPS exposure. (A) HO-1 promoter constructs, HO-1(−4045/+74) and HO-1(−295/+74), were transfected (250 ng/well) in RAW 264.7 cells and promoter activity was analyzed after exposure
    Figure Legend Snippet: TGF-β1 suppresses HO-1 promoter activity during LPS exposure. (A) HO-1 promoter constructs, HO-1(−4045/+74) and HO-1(−295/+74), were transfected (250 ng/well) in RAW 264.7 cells and promoter activity was analyzed after exposure

    Techniques Used: Activity Assay, Construct, Transfection

    4) Product Images from "Extracellular vesicles produced by bone marrow mesenchymal stem cells attenuate renal fibrosis, in part by inhibiting the RhoA/ROCK pathway, in a UUO rat model"

    Article Title: Extracellular vesicles produced by bone marrow mesenchymal stem cells attenuate renal fibrosis, in part by inhibiting the RhoA/ROCK pathway, in a UUO rat model

    Journal: Stem Cell Research & Therapy

    doi: 10.1186/s13287-020-01767-8

    Effects of rhMFGE8 on TGF-β1-induced HK-2 cells. a The protein expressions for α-SMA, E-cadherin, and Fibronectin were detected by Western blot. b The protein levels of α-SMA, E-cadherin, and Fibronectin were expressed as arbitrary densitometric units and normalized by the value of GAPDH. c The levels of IL-1β, IL-6, and TNF-α were detected with ELISA kits. d , g Representative images of HK-2 cells stained with JC-1 and red/green fluorescent ratio in different groups. e , i Representative image of HK-2 cells stained with 2′7′-dichlorodihydrofluorescein diacetate (DCFH-DA). Quantification of DCFH-DA. f , j Rate of cell apoptosis as qualified by flow cytometry. h The ATP content of HK-2 cells in different groups. Scale bar 100 μm. * P
    Figure Legend Snippet: Effects of rhMFGE8 on TGF-β1-induced HK-2 cells. a The protein expressions for α-SMA, E-cadherin, and Fibronectin were detected by Western blot. b The protein levels of α-SMA, E-cadherin, and Fibronectin were expressed as arbitrary densitometric units and normalized by the value of GAPDH. c The levels of IL-1β, IL-6, and TNF-α were detected with ELISA kits. d , g Representative images of HK-2 cells stained with JC-1 and red/green fluorescent ratio in different groups. e , i Representative image of HK-2 cells stained with 2′7′-dichlorodihydrofluorescein diacetate (DCFH-DA). Quantification of DCFH-DA. f , j Rate of cell apoptosis as qualified by flow cytometry. h The ATP content of HK-2 cells in different groups. Scale bar 100 μm. * P

    Techniques Used: Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Flow Cytometry

    Effects of BMSC-EVs on TGF-β1-induced HK-2 cells. a The protein expressions for α-SMA, E-cadherin, and Fibronectin were detected by Western blot. b The protein levels of α-SMA, E-cadherin, and Fibronectin were expressed as arbitrary densitometric units and normalized by the value of GAPDH. c The levels of IL-1β, IL-6, and TNF-α were detected with ELISA kits. d , g Representative images of HK-2 cells stained with JC-1 and red/green fluorescent ratio in different groups. e , i Representative image of HK-2 cells stained with 2′7′-dichlorodihydrofluorescein diacetate (DCFH-DA). Quantification of DCFH-DA. f , j Rate of cell apoptosis as qualified by flow cytometry. h The ATP content of HK-2 cells in different groups. Scale bar 100 μm. * P
    Figure Legend Snippet: Effects of BMSC-EVs on TGF-β1-induced HK-2 cells. a The protein expressions for α-SMA, E-cadherin, and Fibronectin were detected by Western blot. b The protein levels of α-SMA, E-cadherin, and Fibronectin were expressed as arbitrary densitometric units and normalized by the value of GAPDH. c The levels of IL-1β, IL-6, and TNF-α were detected with ELISA kits. d , g Representative images of HK-2 cells stained with JC-1 and red/green fluorescent ratio in different groups. e , i Representative image of HK-2 cells stained with 2′7′-dichlorodihydrofluorescein diacetate (DCFH-DA). Quantification of DCFH-DA. f , j Rate of cell apoptosis as qualified by flow cytometry. h The ATP content of HK-2 cells in different groups. Scale bar 100 μm. * P

    Techniques Used: Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Flow Cytometry

    5) Product Images from "Reversible and irreversible differentiation of cardiac fibroblasts"

    Article Title: Reversible and irreversible differentiation of cardiac fibroblasts

    Journal: Cardiovascular Research

    doi: 10.1093/cvr/cvt338

    Structural adaptations of Fb cells in unrestrained 3-DCMs. ( A ) Fb phenotypes; Rhodamin-Phalloidin (red) marks stress fibres; nuclei stained with DAPI (blue); scale bars represent 10 µm. (a) Round phenotype, (b) dendritic phenotype without stress fibres, (c) dendritic phenotype with stress fibres, and (d)elongated phenotype with stress fibres. ( B ) Quantification of the cell fractions with specific phenotypes in the absence of serum. Fbs in 3-D cultures without mechanical strain and serum acquire a dendritic phenotype without stress fibres. p-MyoFb and non-p-MyoFb acquire an elongated phenotype with stress fibres. ( C ) Contraction of unrestrained 3-DCM by Fb cells. Volume of unrestrained 3-DCM after 3-day cultures. 3-DCMs were populated with: p-MyoFb; Fb pre-treated in 2-D cultures with SD-208 (3 µmol/L); non-p-MyoFb pre-treated with TGF-β1 (400 pmol/L); Fb pre-treated with SD-208 (3 µmol) and TGF-β1(400 pmol/L); Fb pre-treated with Y-27632 (10 µmol/L). No cells represent control 3-DCM without cells. * P
    Figure Legend Snippet: Structural adaptations of Fb cells in unrestrained 3-DCMs. ( A ) Fb phenotypes; Rhodamin-Phalloidin (red) marks stress fibres; nuclei stained with DAPI (blue); scale bars represent 10 µm. (a) Round phenotype, (b) dendritic phenotype without stress fibres, (c) dendritic phenotype with stress fibres, and (d)elongated phenotype with stress fibres. ( B ) Quantification of the cell fractions with specific phenotypes in the absence of serum. Fbs in 3-D cultures without mechanical strain and serum acquire a dendritic phenotype without stress fibres. p-MyoFb and non-p-MyoFb acquire an elongated phenotype with stress fibres. ( C ) Contraction of unrestrained 3-DCM by Fb cells. Volume of unrestrained 3-DCM after 3-day cultures. 3-DCMs were populated with: p-MyoFb; Fb pre-treated in 2-D cultures with SD-208 (3 µmol/L); non-p-MyoFb pre-treated with TGF-β1 (400 pmol/L); Fb pre-treated with SD-208 (3 µmol) and TGF-β1(400 pmol/L); Fb pre-treated with Y-27632 (10 µmol/L). No cells represent control 3-DCM without cells. * P

    Techniques Used: Staining

    Differentiation of Fb cells in 2-D cultures and MRTF-A/B expression. ( A – D ) Different phenotypes, cells are stained for F-actin (a), α-SMA (b), and vinculin (c); scale bars represent 40 µm. ( A ) Spontaneously differentiation to p-MyoFb during 4 days in standard culture medium. ( B ) Treatment with SD-208 (3 µmol/L), an inhibitor for TGF-β-RI kinase, for 4 days maintains the Fb phenotype. ( C ) Treatment with TGF-β1 (400 pmol/L) for 6 days induces non-p-MyoFb. ( D ) Fb cultures are treated simultaneous with SD-208 (3 µmol/L) and TGF-β1 (400 pmol/L) for 4 days. ( E ) Proliferative capacity of cells after 12 days in culture. ( F ) Quantification of immunostained α-SMA-positive cells in different Fb cultures. Western blotting ( G ) of α-SMA in p-MyoFb, SD-208-treated Fb, and Y-27632-treated Fb (4-day-old cultures) and in TGF-β1-treated MyoFb (6-day-old cultures). ( H ) mRNA expression of MRTF-A/B in different Fb phenotypes. * P
    Figure Legend Snippet: Differentiation of Fb cells in 2-D cultures and MRTF-A/B expression. ( A – D ) Different phenotypes, cells are stained for F-actin (a), α-SMA (b), and vinculin (c); scale bars represent 40 µm. ( A ) Spontaneously differentiation to p-MyoFb during 4 days in standard culture medium. ( B ) Treatment with SD-208 (3 µmol/L), an inhibitor for TGF-β-RI kinase, for 4 days maintains the Fb phenotype. ( C ) Treatment with TGF-β1 (400 pmol/L) for 6 days induces non-p-MyoFb. ( D ) Fb cultures are treated simultaneous with SD-208 (3 µmol/L) and TGF-β1 (400 pmol/L) for 4 days. ( E ) Proliferative capacity of cells after 12 days in culture. ( F ) Quantification of immunostained α-SMA-positive cells in different Fb cultures. Western blotting ( G ) of α-SMA in p-MyoFb, SD-208-treated Fb, and Y-27632-treated Fb (4-day-old cultures) and in TGF-β1-treated MyoFb (6-day-old cultures). ( H ) mRNA expression of MRTF-A/B in different Fb phenotypes. * P

    Techniques Used: Expressing, Staining, Western Blot

    6) Product Images from "Kindlin-2 regulates hepatic stellate cells activation and liver fibrogenesis"

    Article Title: Kindlin-2 regulates hepatic stellate cells activation and liver fibrogenesis

    Journal: Cell Death Discovery

    doi: 10.1038/s41420-018-0095-9

    Kindlin-2 promotes Smad2/3 phosphorylation. a LX-2 cells transfected with control siRNA or Kindlin-2 siRNA and further treated with 10 ng/ml TGF-β1 for the indicated time period. P-Smad2/3 and total Smad2/3 levels were detected by western blot. b LX-2 cells transfected with control siRNA or Kindlin-2 siRNA and further treated with 10 ng/ml TGF-β1 for 30 min. The expressions of P-Smad2/3 and total Smad2/3 were determined by immunofluorescence assays. c LX-2 cells were transfected with control vector or Kindlin-2 vector, followed by TGF-β1 (10 ng/ml) treatment for the indicated time period. P-Smad2/3 and total Smad2/3 levels were detected by western blot. d LX-2 cells were transfected with control vector or Kindlin-2 vector, followed by TGF-β1 (10 ng/ml) treatment for 30 min. The expressions of P-Smad2/3 and total Smad2/3 were determined by immunofluorescence assays. The data are representative of three independent experiments. Scale bars = 200 μm
    Figure Legend Snippet: Kindlin-2 promotes Smad2/3 phosphorylation. a LX-2 cells transfected with control siRNA or Kindlin-2 siRNA and further treated with 10 ng/ml TGF-β1 for the indicated time period. P-Smad2/3 and total Smad2/3 levels were detected by western blot. b LX-2 cells transfected with control siRNA or Kindlin-2 siRNA and further treated with 10 ng/ml TGF-β1 for 30 min. The expressions of P-Smad2/3 and total Smad2/3 were determined by immunofluorescence assays. c LX-2 cells were transfected with control vector or Kindlin-2 vector, followed by TGF-β1 (10 ng/ml) treatment for the indicated time period. P-Smad2/3 and total Smad2/3 levels were detected by western blot. d LX-2 cells were transfected with control vector or Kindlin-2 vector, followed by TGF-β1 (10 ng/ml) treatment for 30 min. The expressions of P-Smad2/3 and total Smad2/3 were determined by immunofluorescence assays. The data are representative of three independent experiments. Scale bars = 200 μm

    Techniques Used: Transfection, Western Blot, Immunofluorescence, Plasmid Preparation

    TGF-β1 increases Kindlin-2 expression in HSCs via p38 and ERK MAPK. a Representative western blot analysis of Kindlin-2 from LX-2 cells treated with TGF-β1 (10 ng/ml) for the indicated time period. The right panel shows quantitative analyses of Kindlin-2 after normalization with tubulin. b Representative western blot analysis of Kindlin-2 from LX-2 cells treated with TGF-β1 for 24 h for indicated concentrations. c Quantitative PCR analyses of Kindlin-2 mRNA from LX-2 cells treated with indicated concentrations of TGF-β1 for 24 h (left panel) or 10 ng/ml of TGF-β1 for indicated time intervals (right panel). Western blot ( d ) and immunofluorescence analysis ( e ) of Kindlin-2 from LX-2 cells were treated with or without SP600125 (10 μM), U0126 (1 μM), or SB203580 (1 μM), following TGF-β1 treatment for 24 h. The data are representative of three independent experiments. Scale bars = 200 μm. * p
    Figure Legend Snippet: TGF-β1 increases Kindlin-2 expression in HSCs via p38 and ERK MAPK. a Representative western blot analysis of Kindlin-2 from LX-2 cells treated with TGF-β1 (10 ng/ml) for the indicated time period. The right panel shows quantitative analyses of Kindlin-2 after normalization with tubulin. b Representative western blot analysis of Kindlin-2 from LX-2 cells treated with TGF-β1 for 24 h for indicated concentrations. c Quantitative PCR analyses of Kindlin-2 mRNA from LX-2 cells treated with indicated concentrations of TGF-β1 for 24 h (left panel) or 10 ng/ml of TGF-β1 for indicated time intervals (right panel). Western blot ( d ) and immunofluorescence analysis ( e ) of Kindlin-2 from LX-2 cells were treated with or without SP600125 (10 μM), U0126 (1 μM), or SB203580 (1 μM), following TGF-β1 treatment for 24 h. The data are representative of three independent experiments. Scale bars = 200 μm. * p

    Techniques Used: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Immunofluorescence

    Overexpression of Kindlin-2 promotes TGF-β1-induced HSC activation. a LX-2 cells were transfected with control vector or Kindlin-2 vector followed by TGF-β1 (10 ng/ml) treatment for 48 h. The levels of Kindlin-2, Col1A1, and Fn were determined by western blot analysis. b LX-2 cells were transfected and treated as in a – c . Immunofluorescence assays were performed with anti-Fn and anti-α-SMA antibodies. The data are representative of three independent experiments. Scale bars = 200 μm. * p
    Figure Legend Snippet: Overexpression of Kindlin-2 promotes TGF-β1-induced HSC activation. a LX-2 cells were transfected with control vector or Kindlin-2 vector followed by TGF-β1 (10 ng/ml) treatment for 48 h. The levels of Kindlin-2, Col1A1, and Fn were determined by western blot analysis. b LX-2 cells were transfected and treated as in a – c . Immunofluorescence assays were performed with anti-Fn and anti-α-SMA antibodies. The data are representative of three independent experiments. Scale bars = 200 μm. * p

    Techniques Used: Over Expression, Activation Assay, Transfection, Plasmid Preparation, Western Blot, Immunofluorescence

    Inhibition of Kindlin-2 diminishes the pro-fibrogenic activities of TGF-β1. a LX-2 cells are transfected with control siRNA or Kindlin-2 siRNA followed by TGF-β1 (10 ng/ml) treatment for 48 h. The expressions of Kindlin-2, Col1A1, and Fn were determined by western blot. b – d After transfection with control siRNA or Kindlin-2 siRNA, LX-2 cells were treated with or without TGF-β1 (10 ng/ml) treatment for 24 h. Real-time PCR analyses of Fn, Col1A1, and α-SMA mRNA were performed. e Immunofluorescence analysis of Fn and α-SMA from LX-2 cells that were transfected with control siRNA or Kindlin-2 siRNA and then treated with or without 10 ng/ml TGF-β1 for 48 h. The data are representative of three independent experiments. Scale bars = 200 μm. * p
    Figure Legend Snippet: Inhibition of Kindlin-2 diminishes the pro-fibrogenic activities of TGF-β1. a LX-2 cells are transfected with control siRNA or Kindlin-2 siRNA followed by TGF-β1 (10 ng/ml) treatment for 48 h. The expressions of Kindlin-2, Col1A1, and Fn were determined by western blot. b – d After transfection with control siRNA or Kindlin-2 siRNA, LX-2 cells were treated with or without TGF-β1 (10 ng/ml) treatment for 24 h. Real-time PCR analyses of Fn, Col1A1, and α-SMA mRNA were performed. e Immunofluorescence analysis of Fn and α-SMA from LX-2 cells that were transfected with control siRNA or Kindlin-2 siRNA and then treated with or without 10 ng/ml TGF-β1 for 48 h. The data are representative of three independent experiments. Scale bars = 200 μm. * p

    Techniques Used: Inhibition, Transfection, Western Blot, Real-time Polymerase Chain Reaction, Immunofluorescence

    7) Product Images from "Activated Cardiac Fibroblasts Control Contraction of Human Fibrotic Cardiac Microtissues by a β-Adrenoreceptor-Dependent Mechanism"

    Article Title: Activated Cardiac Fibroblasts Control Contraction of Human Fibrotic Cardiac Microtissues by a β-Adrenoreceptor-Dependent Mechanism

    Journal: Cells

    doi: 10.3390/cells9051270

    TGF-β1 induces fibrotic phenotype in cardiac microtissues. Immunohistochemistry of iCMs:fCFs microtissues cultured in the presence or absence of TGF-β1 (10 ng/mL) at day 10. Panel ( A ) illustrates representative staining for the indicated proteins at the indicated condition (bar = 50 μm). Higher magnification pictures are available in the Supplementary Materials ( Figure S3 ). Panel ( B ) shows quantification of the respective staining for microtissues cultured in the presence (red) or absence (black) of TGF-β1. Graphs show cumulative data of 3 independent experiments. Each triangle represents data for one microtissue. p values were calculated with the Student’s t -test.
    Figure Legend Snippet: TGF-β1 induces fibrotic phenotype in cardiac microtissues. Immunohistochemistry of iCMs:fCFs microtissues cultured in the presence or absence of TGF-β1 (10 ng/mL) at day 10. Panel ( A ) illustrates representative staining for the indicated proteins at the indicated condition (bar = 50 μm). Higher magnification pictures are available in the Supplementary Materials ( Figure S3 ). Panel ( B ) shows quantification of the respective staining for microtissues cultured in the presence (red) or absence (black) of TGF-β1. Graphs show cumulative data of 3 independent experiments. Each triangle represents data for one microtissue. p values were calculated with the Student’s t -test.

    Techniques Used: Immunohistochemistry, Cell Culture, Staining

    Pharmacological targeting of microtissues with TGF-βR1 inhibitor SD208. ( A – D ) iCMs:fCFs microtissues were cultured in the presence or absence of TGF-β1 (10 ng/mL) and SD208 (10 µg/mL). Panel ( A ) shows changes in size of microtissues and panel ( B ) normalized levels of secreted procollagen I (measured by ELISA in supernatants) at the indicated conditions at day 10. Each dot represents data for one microtissue. p values were calculated with ANOVA followed by uncorrected Fisher’s LSD tests for selected groups, * p
    Figure Legend Snippet: Pharmacological targeting of microtissues with TGF-βR1 inhibitor SD208. ( A – D ) iCMs:fCFs microtissues were cultured in the presence or absence of TGF-β1 (10 ng/mL) and SD208 (10 µg/mL). Panel ( A ) shows changes in size of microtissues and panel ( B ) normalized levels of secreted procollagen I (measured by ELISA in supernatants) at the indicated conditions at day 10. Each dot represents data for one microtissue. p values were calculated with ANOVA followed by uncorrected Fisher’s LSD tests for selected groups, * p

    Techniques Used: Cell Culture, Enzyme-linked Immunosorbent Assay

    Contractile properties of cardiac microtissues containing foetal or adult cardiac fibroblasts. Panel (A) shows quantification of contraction parameters of iCMs:fCFs microtissues cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) at day 10. Quantification of contraction parameters of microtissues containing fCFs pretreated with TGF-β1 for 3 days prior microtissue formation (blue) or untreated fCFs (black) recorded at day 10 are shown in panel (B). Each dot represents average data of one experiment. Data of individual experiments are available in the Supplementary Materials ( Figures S5 and S8 ). p values were calculated with the paired Student’s t -test. Panel (C) shows quantification of contraction parameters of cardiac microtissues containing aCFs from unaffected hearts (white) or heart failure (HF) patients (grey). Each dot represents average data of one experiment ( n = 14–18). p values were calculated with the Student’s t -test. Representative contraction records are available in the Supplementary Materials ( Figures S5, S10B and S11 and Videos S2–S6 ).
    Figure Legend Snippet: Contractile properties of cardiac microtissues containing foetal or adult cardiac fibroblasts. Panel (A) shows quantification of contraction parameters of iCMs:fCFs microtissues cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) at day 10. Quantification of contraction parameters of microtissues containing fCFs pretreated with TGF-β1 for 3 days prior microtissue formation (blue) or untreated fCFs (black) recorded at day 10 are shown in panel (B). Each dot represents average data of one experiment. Data of individual experiments are available in the Supplementary Materials ( Figures S5 and S8 ). p values were calculated with the paired Student’s t -test. Panel (C) shows quantification of contraction parameters of cardiac microtissues containing aCFs from unaffected hearts (white) or heart failure (HF) patients (grey). Each dot represents average data of one experiment ( n = 14–18). p values were calculated with the Student’s t -test. Representative contraction records are available in the Supplementary Materials ( Figures S5, S10B and S11 and Videos S2–S6 ).

    Techniques Used: Cell Culture

    Cardiac microtissue electrophysiology. iCMs:fCFs microtissues were cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) for 10 days. Panel ( A ) shows quantifications of the contraction parameters recorded during spontaneous contractile activity (triangles, ctr) and then upon electrical stimulation with 3 Hz (circles, 3 Hz). Each dot represents data for one microtissue at the indicated condition, lines match data obtained from the same microtissue. p values were calculated with the paired Student’s t -test. Panel ( B ) illustrates representative action potentials recorded with FluoVolt probe (left) and the respective contractions (right). Quantifications of action potential parameters are shown in panel ( C ). Graphs show cumulative data of 3 independent experiments. Each dot represents data for one microtissue. p values were calculated with the Student’s t -test. APD—action potential duration, TRise—depolarisation phase.
    Figure Legend Snippet: Cardiac microtissue electrophysiology. iCMs:fCFs microtissues were cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) for 10 days. Panel ( A ) shows quantifications of the contraction parameters recorded during spontaneous contractile activity (triangles, ctr) and then upon electrical stimulation with 3 Hz (circles, 3 Hz). Each dot represents data for one microtissue at the indicated condition, lines match data obtained from the same microtissue. p values were calculated with the paired Student’s t -test. Panel ( B ) illustrates representative action potentials recorded with FluoVolt probe (left) and the respective contractions (right). Quantifications of action potential parameters are shown in panel ( C ). Graphs show cumulative data of 3 independent experiments. Each dot represents data for one microtissue. p values were calculated with the Student’s t -test. APD—action potential duration, TRise—depolarisation phase.

    Techniques Used: Cell Culture, Activity Assay

    TGF-β1 activates foetal cardiac fibroblasts in microtissues. Panel ( A ) demonstrates changes in size of microtissues generated with fCFs only (fCFs, left) and iCMs mixed with fCFs in ratio 4:1 (iCMs:fCFs, right) cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) for 10 days. Panel ( B ) shows relative levels of procollagen I (measured by ELISA), at day 10 in supernatants of all three microtissue types: fCFs (left), iCMs:fCFs (middle) and iCMs (right). Graphs show cumulative data of 2–5 independent experiments. Each dot represents data of one microtissue. Panel ( C ) illustrates representative picrosirius red staining in iCMs:fCFs microtissues at day 10 (bar = 10 μm). Panel ( D ) shows caspase 3/7 activity measured at day 10 in iCMs:fCFs microtissues. Graphs show cumulative data of 3 independent experiments. Panel ( E ) shows IL-6 levels measured by ELISA, at day 10 in supernatants of iCMs:fCFs microtissues. Graphs show cumulative data of 3 independent experiments. Each triangle represents data of one microtissue. Panel ( F ) summarizes fold changes in gene expression in indicated microtissues in the presence of TGF-β1 (in relation to expression in the absence of TGF-β1). * p
    Figure Legend Snippet: TGF-β1 activates foetal cardiac fibroblasts in microtissues. Panel ( A ) demonstrates changes in size of microtissues generated with fCFs only (fCFs, left) and iCMs mixed with fCFs in ratio 4:1 (iCMs:fCFs, right) cultured in the presence (red) or absence (black) of TGF-β1 (10 ng/mL) for 10 days. Panel ( B ) shows relative levels of procollagen I (measured by ELISA), at day 10 in supernatants of all three microtissue types: fCFs (left), iCMs:fCFs (middle) and iCMs (right). Graphs show cumulative data of 2–5 independent experiments. Each dot represents data of one microtissue. Panel ( C ) illustrates representative picrosirius red staining in iCMs:fCFs microtissues at day 10 (bar = 10 μm). Panel ( D ) shows caspase 3/7 activity measured at day 10 in iCMs:fCFs microtissues. Graphs show cumulative data of 3 independent experiments. Panel ( E ) shows IL-6 levels measured by ELISA, at day 10 in supernatants of iCMs:fCFs microtissues. Graphs show cumulative data of 3 independent experiments. Each triangle represents data of one microtissue. Panel ( F ) summarizes fold changes in gene expression in indicated microtissues in the presence of TGF-β1 (in relation to expression in the absence of TGF-β1). * p

    Techniques Used: Generated, Cell Culture, Enzyme-linked Immunosorbent Assay, Staining, Activity Assay, Expressing

    8) Product Images from "EGFR Signaling Is Required for TGF-β1–Mediated COX-2 Induction in Human Bronchial Epithelial Cells"

    Article Title: EGFR Signaling Is Required for TGF-β1–Mediated COX-2 Induction in Human Bronchial Epithelial Cells

    Journal:

    doi: 10.1165/rcmb.2007-0100OC

    TGF-β1 and EGF induce COX-2 at the transcriptional and post-transcriptional levels in HBECs. ( A ) HBEC3 cells were transfected with COX-2 promoter (−1437/+127)-Luc and pRL-TK. Twenty-four hours after the transfection, cells were
    Figure Legend Snippet: TGF-β1 and EGF induce COX-2 at the transcriptional and post-transcriptional levels in HBECs. ( A ) HBEC3 cells were transfected with COX-2 promoter (−1437/+127)-Luc and pRL-TK. Twenty-four hours after the transfection, cells were

    Techniques Used: Transfection

    Possible mechanisms of COX-2 induction by TGF-β and EGF in HBECs. TGF-β1 activates Smad3 and increases COX-2 transcription. EGF predominantly increases the stability of COX-2 mRNA and causes a minor increase in COX-2 transcription. Combined
    Figure Legend Snippet: Possible mechanisms of COX-2 induction by TGF-β and EGF in HBECs. TGF-β1 activates Smad3 and increases COX-2 transcription. EGF predominantly increases the stability of COX-2 mRNA and causes a minor increase in COX-2 transcription. Combined

    Techniques Used:

    Smad3 and ERK phosphorylation mediate COX-2 induction after exposure of HBEC to TGF-β1. ( A–D ) HBECs were transfected with siRNA SMARTpool for Smad3 (100 nM, A , B ) or Smad2 (50 nM, C , D ). Forty-eight hours after the transfection, TGF-β1
    Figure Legend Snippet: Smad3 and ERK phosphorylation mediate COX-2 induction after exposure of HBEC to TGF-β1. ( A–D ) HBECs were transfected with siRNA SMARTpool for Smad3 (100 nM, A , B ) or Smad2 (50 nM, C , D ). Forty-eight hours after the transfection, TGF-β1

    Techniques Used: Transfection

    Inhibition of EGF receptor (EGFR) signaling blocks TGF-β1–mediated COX-2 induction. HBEC3 cells were pretreated with ( A ) PD153035 (EGFR inhibitor, 0.5μM), ( B ) AG1478 (EGFR inhibitor, 0.5μM), or one of the following neutralizing
    Figure Legend Snippet: Inhibition of EGF receptor (EGFR) signaling blocks TGF-β1–mediated COX-2 induction. HBEC3 cells were pretreated with ( A ) PD153035 (EGFR inhibitor, 0.5μM), ( B ) AG1478 (EGFR inhibitor, 0.5μM), or one of the following neutralizing

    Techniques Used: Inhibition

    HBEC3 cells maintain a constitutive level of EGFR phosphorylation, which is inhibited by the EGFR inhibitor, PD153035, or neutralizing antibodies against EGFR or amphiregulin. ( A ) HBEC3 cells were treated with 5 ng/ml TGF-β1 or 50 ng/ml EGF, and
    Figure Legend Snippet: HBEC3 cells maintain a constitutive level of EGFR phosphorylation, which is inhibited by the EGFR inhibitor, PD153035, or neutralizing antibodies against EGFR or amphiregulin. ( A ) HBEC3 cells were treated with 5 ng/ml TGF-β1 or 50 ng/ml EGF, and

    Techniques Used:

    Epidermal growth factor (EGF) potentiates transforming growth factor (TGF)-β1–mediated cyclooxygenase (COX)-2 induction in human bronchial epithelial cells (HBECs). HBEC3 cells were cultured in 6-well plates and treated with TGF-β1
    Figure Legend Snippet: Epidermal growth factor (EGF) potentiates transforming growth factor (TGF)-β1–mediated cyclooxygenase (COX)-2 induction in human bronchial epithelial cells (HBECs). HBEC3 cells were cultured in 6-well plates and treated with TGF-β1

    Techniques Used: Cell Culture

    9) Product Images from "MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model"

    Article Title: MicroRNA-29b Mediates Lung Mesenchymal-Epithelial Transition and Prevents Lung Fibrosis in the Silicosis Model

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2018.10.017

    miR-29b Inhibitor Enhanced the Development of EMT in RLE-6TN Cells After silica (TGF-β1) treatment for 24 hr, the RLE-6TN cells were incubated with silica (TGF-β1) plus miR-29b inhibitor or inhibitor NC for another 24 hr. (A) The transfection efficiency was greater than 80% of the RLE-6TN cells transfected with Cy3-labeled miR-29b inhibitor, and qPCR analysis revealed that miR-29b inhibitor markedly decreased the level of miR-29b in RLE-6TN cells. (B) qPCR analysis showed that miR-29b inhibitor increased the level of COL1A1 compared with the silica + inhibitor NC group but did not alter the levels of CDH1 and VIM. (C) qPCR for snai1 revealed similar results as with COL1A1. (D) miR-29b inhibitor decreased the ratio of E-cadherin:vimentin. (E) The results of qPCR showed that miR-29b inhibitor downregulated the expression of CDH1 but upregulated the expression of VIM, α-SMA, and COL1A1 in the TGF-β1 EMT model. (F) miR-29b inhibitor also decreased the ratio of E-cadherin:vimentin in the TGF-β1 EMT model. All results were replicated at least three times independently. The data are presented as means ± SD. * p
    Figure Legend Snippet: miR-29b Inhibitor Enhanced the Development of EMT in RLE-6TN Cells After silica (TGF-β1) treatment for 24 hr, the RLE-6TN cells were incubated with silica (TGF-β1) plus miR-29b inhibitor or inhibitor NC for another 24 hr. (A) The transfection efficiency was greater than 80% of the RLE-6TN cells transfected with Cy3-labeled miR-29b inhibitor, and qPCR analysis revealed that miR-29b inhibitor markedly decreased the level of miR-29b in RLE-6TN cells. (B) qPCR analysis showed that miR-29b inhibitor increased the level of COL1A1 compared with the silica + inhibitor NC group but did not alter the levels of CDH1 and VIM. (C) qPCR for snai1 revealed similar results as with COL1A1. (D) miR-29b inhibitor decreased the ratio of E-cadherin:vimentin. (E) The results of qPCR showed that miR-29b inhibitor downregulated the expression of CDH1 but upregulated the expression of VIM, α-SMA, and COL1A1 in the TGF-β1 EMT model. (F) miR-29b inhibitor also decreased the ratio of E-cadherin:vimentin in the TGF-β1 EMT model. All results were replicated at least three times independently. The data are presented as means ± SD. * p

    Techniques Used: Incubation, Transfection, Labeling, Real-time Polymerase Chain Reaction, Expressing

    miR-29b Mimics Promoted MET and Reversed EMT in RLE-6TN Cells After being incubated with silica (TGF-β1) for 24 hr, the RLE-6TN cells were incubated with silica (TGF-β1) in addition to miR-29b mimics or mimic negative control (NC) for an additional 24 hr. (A) The transfection efficiency was greater than 80% of the RLE-6TN cells transfected with Cy3-labeled miR-29b mimics, and qPCR analysis revealed that miR-29b mimics markedly increased the level of miR-29b in RLE-6TN cells. (B) qPCR analysis showed that miR-29b mimics increased the level of CDH1 and decreased the levels of VIM and α-SMA. (C) The results of qPCR suggested that miR-29b mimics did not alter the level of snai1. (D) Western blot analysis revealed that miR-29b mimics increased the ratio of E-cadherin:vimentin significantly in RLE-6TN cells. (E) TGF-β1 induced the downregulation of CDH1 expression and upregulation of VIM and α-SMA in RLE-6TN cells. (F) TGF-β1 induced the downregulation of miR-29b. (G) qPCR analysis showed that miR-29b mimics decreased the levels of VIM, α-SMA, COL1A1, and Tgfb1 compared with the TGF-β1 + mimic NC group. (H) Western blot analysis confirmed that miR-29b mimics increased the ratio of E-cadherin:vimentin significantly in the classical EMT model. All results were replicated at least three times independently. The data are presented as means ± SD. * p
    Figure Legend Snippet: miR-29b Mimics Promoted MET and Reversed EMT in RLE-6TN Cells After being incubated with silica (TGF-β1) for 24 hr, the RLE-6TN cells were incubated with silica (TGF-β1) in addition to miR-29b mimics or mimic negative control (NC) for an additional 24 hr. (A) The transfection efficiency was greater than 80% of the RLE-6TN cells transfected with Cy3-labeled miR-29b mimics, and qPCR analysis revealed that miR-29b mimics markedly increased the level of miR-29b in RLE-6TN cells. (B) qPCR analysis showed that miR-29b mimics increased the level of CDH1 and decreased the levels of VIM and α-SMA. (C) The results of qPCR suggested that miR-29b mimics did not alter the level of snai1. (D) Western blot analysis revealed that miR-29b mimics increased the ratio of E-cadherin:vimentin significantly in RLE-6TN cells. (E) TGF-β1 induced the downregulation of CDH1 expression and upregulation of VIM and α-SMA in RLE-6TN cells. (F) TGF-β1 induced the downregulation of miR-29b. (G) qPCR analysis showed that miR-29b mimics decreased the levels of VIM, α-SMA, COL1A1, and Tgfb1 compared with the TGF-β1 + mimic NC group. (H) Western blot analysis confirmed that miR-29b mimics increased the ratio of E-cadherin:vimentin significantly in the classical EMT model. All results were replicated at least three times independently. The data are presented as means ± SD. * p

    Techniques Used: Incubation, Negative Control, Transfection, Labeling, Real-time Polymerase Chain Reaction, Western Blot, Expressing

    10) Product Images from "A novel molecular pathway for Snail-dependent, SPARC-mediated invasion in non-small cell lung cancer pathogenesis"

    Article Title: A novel molecular pathway for Snail-dependent, SPARC-mediated invasion in non-small cell lung cancer pathogenesis

    Journal: Cancer prevention research (Philadelphia, Pa.)

    doi: 10.1158/1940-6207.CAPR-13-0263

    TGF-β1 is upregulated by Snail upstream of ERK1/2 and SPARC
    Figure Legend Snippet: TGF-β1 is upregulated by Snail upstream of ERK1/2 and SPARC

    Techniques Used:

    11) Product Images from "Equine CD4+ CD25high T cells exhibit regulatory activity by close contact and cytokine-dependent mechanisms in vitro"

    Article Title: Equine CD4+ CD25high T cells exhibit regulatory activity by close contact and cytokine-dependent mechanisms in vitro

    Journal: Immunology

    doi: 10.1111/j.1365-2567.2011.03489.x

    Strategy of in-vitro induction and expansion of CD4 + CD25 + T cells. Freshly isolated peripheral blood mononuclear cells (PBMC) from healthy horses were sorted according to their double expression of CD4 and CD25. To enrich maximally for forkhead box P3 (FoxP3) + cells, the CD25 high gate was set to incorporate only the top 3% of all CD4 + T cells with the brightest fluorescence signal for CD25. The sorted CD4 + CD25 − (n/0), CD4 + CD25 dim (d/0) and CD4 + CD25 high (h/0) cells were cultured with a combination of recombinant human interleukin-2 (rh.IL-2), rh.TGF-β1 and concanavalin A (ConA) (cocktail). Four days later, resorting of the stimulated CD4 + CD25 − cells was performed and percentages of induced CD4 + CD25 dim ( i d), CD4 + CD25 high ( i h) cells as well as remaining CD25 − (n) cells were measured.
    Figure Legend Snippet: Strategy of in-vitro induction and expansion of CD4 + CD25 + T cells. Freshly isolated peripheral blood mononuclear cells (PBMC) from healthy horses were sorted according to their double expression of CD4 and CD25. To enrich maximally for forkhead box P3 (FoxP3) + cells, the CD25 high gate was set to incorporate only the top 3% of all CD4 + T cells with the brightest fluorescence signal for CD25. The sorted CD4 + CD25 − (n/0), CD4 + CD25 dim (d/0) and CD4 + CD25 high (h/0) cells were cultured with a combination of recombinant human interleukin-2 (rh.IL-2), rh.TGF-β1 and concanavalin A (ConA) (cocktail). Four days later, resorting of the stimulated CD4 + CD25 − cells was performed and percentages of induced CD4 + CD25 dim ( i d), CD4 + CD25 high ( i h) cells as well as remaining CD25 − (n) cells were measured.

    Techniques Used: In Vitro, Isolation, Expressing, Fluorescence, Cell Culture, Recombinant

    12) Product Images from "Smad4 in T cells plays a protective role in the development of autoimmune Sjögren's syndrome in the nonobese diabetic mouse"

    Article Title: Smad4 in T cells plays a protective role in the development of autoimmune Sjögren's syndrome in the nonobese diabetic mouse

    Journal: Oncotarget

    doi: 10.18632/oncotarget.13437

    Teff cells from Smad4 tKO NOD mice have restricted sensitivity to Treg cells A. CFSE-labelled Teff cells from WT or Smad4 tKO NOD mice were stimulated (Stim) with anti-CD3/CD28-coated beads for 72 h in the presence of Treg cells from WT NOD mice at various ratios (left margin). Proliferation of Teff cells was assessed by flow cytometry. B. The percentage of cells undergoing the indicated number of divisions when the Treg:Teff cell ratio was 1:1. C. CFSE-labelled Teff cells were stimulated (Stim) with anti-CD3/CD28-coated beads for 72 h with or without TGF-β1 (1 or 10 ng/ml) and analyzed by flow cytometry. D. The percentage of cells undergoing the indicated number of divisions when exposed to 10 ng/ml of TGF-β1. Values are means ± SD ( n = 3-4/group), * P
    Figure Legend Snippet: Teff cells from Smad4 tKO NOD mice have restricted sensitivity to Treg cells A. CFSE-labelled Teff cells from WT or Smad4 tKO NOD mice were stimulated (Stim) with anti-CD3/CD28-coated beads for 72 h in the presence of Treg cells from WT NOD mice at various ratios (left margin). Proliferation of Teff cells was assessed by flow cytometry. B. The percentage of cells undergoing the indicated number of divisions when the Treg:Teff cell ratio was 1:1. C. CFSE-labelled Teff cells were stimulated (Stim) with anti-CD3/CD28-coated beads for 72 h with or without TGF-β1 (1 or 10 ng/ml) and analyzed by flow cytometry. D. The percentage of cells undergoing the indicated number of divisions when exposed to 10 ng/ml of TGF-β1. Values are means ± SD ( n = 3-4/group), * P

    Techniques Used: Mouse Assay, Flow Cytometry, Cytometry

    13) Product Images from "Suitable parameter choice on quantitative morphology of A549 cell in epithelial–mesenchymal transition"

    Article Title: Suitable parameter choice on quantitative morphology of A549 cell in epithelial–mesenchymal transition

    Journal: Bioscience Reports

    doi: 10.1042/BSR20150070

    Images of cell shape in segment pre-and post ( A ) An image with points of grid stimulated by TGF-β1. ( B ) An image with points of grid never stimulated by TGF-β1. ( C ) The image stimulated by TGF-β1 with segmented and sorted cells. ( D ) The image stimulated never by TGF-β1, with segmented and sorted cells. The images were captured by phase contrast microscope (Olympus CKX41-A32PH, Tokyo, Japan) with a LCACHN20XPH 20×/0.4 NA objective (bars, 20 μm).
    Figure Legend Snippet: Images of cell shape in segment pre-and post ( A ) An image with points of grid stimulated by TGF-β1. ( B ) An image with points of grid never stimulated by TGF-β1. ( C ) The image stimulated by TGF-β1 with segmented and sorted cells. ( D ) The image stimulated never by TGF-β1, with segmented and sorted cells. The images were captured by phase contrast microscope (Olympus CKX41-A32PH, Tokyo, Japan) with a LCACHN20XPH 20×/0.4 NA objective (bars, 20 μm).

    Techniques Used: Microscopy

    Choosing, shape depiction and segmentation of cells in images ( A ) An original image stimulated by TGF-β1. ( B ) The image with points of grid and chosen cells filled with black. ( C ) Segmented cells in the image stimulated by TGF-β1. The images were captured by phase contrast microscope (Olympus CKX41-A32PH, Tokyo, Japan) with a CPLN10XPH 10×/0.25 NA objective (bars, 40 μm).
    Figure Legend Snippet: Choosing, shape depiction and segmentation of cells in images ( A ) An original image stimulated by TGF-β1. ( B ) The image with points of grid and chosen cells filled with black. ( C ) Segmented cells in the image stimulated by TGF-β1. The images were captured by phase contrast microscope (Olympus CKX41-A32PH, Tokyo, Japan) with a CPLN10XPH 10×/0.25 NA objective (bars, 40 μm).

    Techniques Used: Microscopy

    Nine parameters on cellular shape compared between TGF-β1-treated group and TGF-β1-untreated group Between TGF-β1-treated group (cell numbers=1267) and TGF-β1-untreated group (cell numbers=1832), nine morphological parameters as area/box ( A ), aspect ( B ), axis major ( C ), box X / Y ( D ), diameter max ( E ), diameter min ( F ), radius min ( G ), radius ratio ( H ) and roundness ( I ) showed statistically difference ( P
    Figure Legend Snippet: Nine parameters on cellular shape compared between TGF-β1-treated group and TGF-β1-untreated group Between TGF-β1-treated group (cell numbers=1267) and TGF-β1-untreated group (cell numbers=1832), nine morphological parameters as area/box ( A ), aspect ( B ), axis major ( C ), box X / Y ( D ), diameter max ( E ), diameter min ( F ), radius min ( G ), radius ratio ( H ) and roundness ( I ) showed statistically difference ( P

    Techniques Used:

    14) Product Images from "Nrf2 inhibits epithelial-mesenchymal transition by suppressing snail expression during pulmonary fibrosis"

    Article Title: Nrf2 inhibits epithelial-mesenchymal transition by suppressing snail expression during pulmonary fibrosis

    Journal: Scientific Reports

    doi: 10.1038/srep38646

    Activating Nrf2 attenuated TGF-β1-induced EMT in RLE-6TN cells. ( A ) Rats RLE-6TN cells were treated with SFN (0–10 μmol/L) for 24 h and the nuclear expression of Nrf2 was measured by Western blot. The representative bands were obtained from different gels for repeated experiments. Histone H3 was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), ++ P
    Figure Legend Snippet: Activating Nrf2 attenuated TGF-β1-induced EMT in RLE-6TN cells. ( A ) Rats RLE-6TN cells were treated with SFN (0–10 μmol/L) for 24 h and the nuclear expression of Nrf2 was measured by Western blot. The representative bands were obtained from different gels for repeated experiments. Histone H3 was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), ++ P

    Techniques Used: Expressing, Western Blot

    Nrf2 inhibited the development of EMT via suppressing the expression of snail. Snail siRNA were transfected in RLE-6TN cells, after 6 h incubation, the cells were treated with SFN for 24 h, followed by stimulation with TGF-β1 for 24 h. Cell lysates were collected and the relative proteins were determined by Western blot. The representative bands were obtained from different gels for repeated experiments. β-actin was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), **P
    Figure Legend Snippet: Nrf2 inhibited the development of EMT via suppressing the expression of snail. Snail siRNA were transfected in RLE-6TN cells, after 6 h incubation, the cells were treated with SFN for 24 h, followed by stimulation with TGF-β1 for 24 h. Cell lysates were collected and the relative proteins were determined by Western blot. The representative bands were obtained from different gels for repeated experiments. β-actin was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), **P

    Techniques Used: Expressing, Transfection, Incubation, Western Blot

    Silencing Nrf2 enhanced TGF-β1-induced EMT in RLE-6TN cells. Nrf2 siRNA were transfected in cells before stimulated with TGF-β1 for 24 h, then cell lysates were collected and the relative proteins were determined by Western blot. The representative bands were obtained from different gels for repeated experiments. β-actin was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), **P
    Figure Legend Snippet: Silencing Nrf2 enhanced TGF-β1-induced EMT in RLE-6TN cells. Nrf2 siRNA were transfected in cells before stimulated with TGF-β1 for 24 h, then cell lysates were collected and the relative proteins were determined by Western blot. The representative bands were obtained from different gels for repeated experiments. β-actin was used as an internal reference for relative quantification. Data were expressed as mean ± SD (n = 3–4 per group), **P

    Techniques Used: Transfection, Western Blot

    15) Product Images from "Posttreatment with Protectin DX ameliorates bleomycin-induced pulmonary fibrosis and lung dysfunction in mice"

    Article Title: Posttreatment with Protectin DX ameliorates bleomycin-induced pulmonary fibrosis and lung dysfunction in mice

    Journal: Scientific Reports

    doi: 10.1038/srep46754

    PDX repressed EMT in vivo and in vitro . Mice were treated with saline or bleomycin (BLM) intratracheally (i.t.) at 2.0 mg/kg on day 0. From day 8, posttreatment with Protectin DX (PDX) (1 μg/mouse) intraperitoneally (i.p.) followed by boosted 100 ng/mouse every two days. Lungs were removed on day 21 after BLM challenge to measure the protein expression of EMT markers by immunohistochemistry (x400) (brown cells represented positive cells) ( A – P ) and Western blot ( Q – S ). Primary rats alveolar type II epithelial (ATII) cells were administrated with TGF-β1 (10 nM) followed by different concentration of PDX (100 nM, 10 nM, 1 nM) for 48 h to detect the expression of EMT markers including α-SMA, N-cadherin, and E-cadherin protein by western blot (T-Y). Data are presented as mean ± SEM. ns: not significant, *P
    Figure Legend Snippet: PDX repressed EMT in vivo and in vitro . Mice were treated with saline or bleomycin (BLM) intratracheally (i.t.) at 2.0 mg/kg on day 0. From day 8, posttreatment with Protectin DX (PDX) (1 μg/mouse) intraperitoneally (i.p.) followed by boosted 100 ng/mouse every two days. Lungs were removed on day 21 after BLM challenge to measure the protein expression of EMT markers by immunohistochemistry (x400) (brown cells represented positive cells) ( A – P ) and Western blot ( Q – S ). Primary rats alveolar type II epithelial (ATII) cells were administrated with TGF-β1 (10 nM) followed by different concentration of PDX (100 nM, 10 nM, 1 nM) for 48 h to detect the expression of EMT markers including α-SMA, N-cadherin, and E-cadherin protein by western blot (T-Y). Data are presented as mean ± SEM. ns: not significant, *P

    Techniques Used: In Vivo, In Vitro, Mouse Assay, Expressing, Immunohistochemistry, Western Blot, Concentration Assay

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    Article Snippet: .. Recombinant mature TGF-β1 was from PeproTech EC Ltd, London, UK. .. Cloning and Recombinant Protein Expression —The plasmid pcDNA3-HA-hHMGA2ΔC (amino acids 1–83) was cloned by PCR into the vector pcDNA3-HA C-terminally of the HA tag using the EcoRI and XhoI restriction sites.

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    Article Snippet: To up-regulate Bcl11b expression in vitro , cells were transfected with 4 µg of mouse Bcl11b plasmid (GeneChem, Shanghai, China) using Amaxa Nucleofector Kit (Lonza, Basel, Switzerland). .. For TGF-β1 treatment, recombinant TGF-β1 (Peprotech, Rocky Hill, NJ, USA) was prepared as a stock solution at a concentration of 0.1 mg/mL in 10 mM citric acid. .. Cells were cultured with 5 µM TGF-β1 in the presence (pBcl11b + TGF-β1 group) or absence (TGF-β1 group) of pBcl11b.

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    Article Snippet: .. Recombinant mature TGF-β1 was purchased from PeproTech. ..

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    Article Snippet: Myelin oligodendrocyte glycoprotein (MOG)35–55 peptide (MEVGWYRSPFSRVVHLYRNGK, purity ≥ 98%) was purchased from GenScript (Nanjing, China). .. Recombinant murine granulocyte–macrophage colony-stimulating factor (rmGM-CSF), recombinant murine IL-4, and recombinant human transforming growth factor β1 (rhTGF-β1) were purchased from PeproTech (Rocky Hill, NJ). .. TGF-β-neutralizing monoclonal IgG1 (aTGF-β, clone: 1D11.16.8) was from Bio X Cell (West Lebanon, NH).

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    Article Title: CCN5 Reduces Ligamentum Flavum Hypertrophy by Modulating the TGF‐β Pathway
    Article Snippet: .. For the both cell types, exogenous recombinant human TGF‐β1 (Peprotech, Rocky Hill, NJ) was added to a 10 ng/ml final concentration in the TGF‐β1 groups, and an equal amount of PBS was added in the control groups. .. The exogeneous TGF‐β1 concentration was determined based on previously published and our Supplementary Data (Supplementary Fig. S1).

    Concentration Assay:

    Article Title: Bcl11b Regulates IL-17 Through the TGF-β/Smad Pathway in HDM-Induced Asthma
    Article Snippet: To up-regulate Bcl11b expression in vitro , cells were transfected with 4 µg of mouse Bcl11b plasmid (GeneChem, Shanghai, China) using Amaxa Nucleofector Kit (Lonza, Basel, Switzerland). .. For TGF-β1 treatment, recombinant TGF-β1 (Peprotech, Rocky Hill, NJ, USA) was prepared as a stock solution at a concentration of 0.1 mg/mL in 10 mM citric acid. .. Cells were cultured with 5 µM TGF-β1 in the presence (pBcl11b + TGF-β1 group) or absence (TGF-β1 group) of pBcl11b.

    Article Title: CCN5 Reduces Ligamentum Flavum Hypertrophy by Modulating the TGF‐β Pathway
    Article Snippet: .. For the both cell types, exogenous recombinant human TGF‐β1 (Peprotech, Rocky Hill, NJ) was added to a 10 ng/ml final concentration in the TGF‐β1 groups, and an equal amount of PBS was added in the control groups. .. The exogeneous TGF‐β1 concentration was determined based on previously published and our Supplementary Data (Supplementary Fig. S1).

    Incubation:

    Article Title: Tumor-associated macrophages promote tumor metastasis via the TGF-β/SOX9 axis in non-small cell lung cancer
    Article Snippet: .. In the experiments, A549 and H1299 cells were incubated with 10 ng/mL of recombinant human TGF-β (100-21C, PeproTech) in RPMI-1640 medium for 48 h. To stimulate transformation of THP-1 cells into macrophages, 50 ng/mL PMA (Sigma Chemical) were added to the medium for 48 h; cells were then washed three times with PBS and incubated for another 24 h in the absence of PMA. .. Co-culture procedures THP-1 derived macrophages and lung cancer cells were co-cultured using a cell culture insert (Corning, NY, USA) with a porous membrane to separate the upper and lower chambers.

    Transformation Assay:

    Article Title: Tumor-associated macrophages promote tumor metastasis via the TGF-β/SOX9 axis in non-small cell lung cancer
    Article Snippet: .. In the experiments, A549 and H1299 cells were incubated with 10 ng/mL of recombinant human TGF-β (100-21C, PeproTech) in RPMI-1640 medium for 48 h. To stimulate transformation of THP-1 cells into macrophages, 50 ng/mL PMA (Sigma Chemical) were added to the medium for 48 h; cells were then washed three times with PBS and incubated for another 24 h in the absence of PMA. .. Co-culture procedures THP-1 derived macrophages and lung cancer cells were co-cultured using a cell culture insert (Corning, NY, USA) with a porous membrane to separate the upper and lower chambers.

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  • 99
    PeproTech tgf β 1
    Puerarin inhibited <t>TGF-β1-induced</t> HUVECs migration rate . HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- <t>β</t> 1 (10 ng/ml) for 48 h until a monolayer was formed. Scratches were made straightly across the dishes. After rinsing twice, the medium was replaced by RPMI1640 with no FBS. Photographs were taken at indicated times (scale bars: 50 μ m).
    Tgf β 1, supplied by PeproTech, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    PeproTech recombinant human tgf β1
    ALK4/5/7 inhibitor and <t>TGF-β</t> neutralizing antibodies, but not sActRIIB-Fc, effectively block SMAD2/3 signaling upon fluid flow stimulation. a ALK4/5/7 inhibitor (LY-364947; n = 3) significantly reduces baseline and fluid flow increased expression of Pai1, Fn1, Col1a1, Ptgs2, and Snai1 while the expression of Snai2 is less decreased. b TGF-β neutralizing antibodies (TGF-β Ab; n = 3) inhibited fluid flow-induced expression of SMAD2/3 target genes ( Pai1 and Fn1 ), while c soluble activin type-IIB-receptor fusion protein (sActRIIB-Fc; n = 5) did not. d Combining TGF-β Ab with sActRIIB-Fc ( n = 4) did not further increase the inhibitory effect. e <t>TGF-β1</t> ( n = 2) or activin B ( n = 3) ligand-induced Pai1 expression was effectively inhibited by TGF-β Ab or sActRIIB-Fc, respectively ( t = 4 h). Parallel plate flow chamber induced fluid shear stress in PTECs at t = 16 h ( a – d ); qPCR, Hprt served as housekeeping gene to correct for cDNA input; data normalized to unstimulated controls (fold change); n = 2–5 per condition as indicated. * P
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    PeproTech th17 conditions
    3.1. <t>Th17</t> and Th1 cells are found in the K/BxN arthritis model
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    PeproTech human tgf β1
    Effects of thalidomide (THD) on morphological transformation of myofibroblast (MF) induced by transforming growth factor <t>(TGF)-β1.</t> Human fetal lung fibroblast (HFL-F) were incubated for 4 days with 0·1% fetal bovine serum (a), TGF-β1
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    Puerarin inhibited TGF-β1-induced HUVECs migration rate . HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h until a monolayer was formed. Scratches were made straightly across the dishes. After rinsing twice, the medium was replaced by RPMI1640 with no FBS. Photographs were taken at indicated times (scale bars: 50 μ m).

    Journal: PPAR Research

    Article Title: Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition

    doi: 10.1155/2017/2647129

    Figure Lengend Snippet: Puerarin inhibited TGF-β1-induced HUVECs migration rate . HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h until a monolayer was formed. Scratches were made straightly across the dishes. After rinsing twice, the medium was replaced by RPMI1640 with no FBS. Photographs were taken at indicated times (scale bars: 50 μ m).

    Article Snippet: TGF-β 1 was purchased from PEPROTECH (100-21C).

    Techniques: Migration

    Puerarin inhibited Smad2 phosphorylation in HUVECs. HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. Protein levels of p-Smad2 and Smad2 in cell lysates in indicated groups were detected by WB, normalized to GAPDH ( n = 6). ∗ p

    Journal: PPAR Research

    Article Title: Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition

    doi: 10.1155/2017/2647129

    Figure Lengend Snippet: Puerarin inhibited Smad2 phosphorylation in HUVECs. HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. Protein levels of p-Smad2 and Smad2 in cell lysates in indicated groups were detected by WB, normalized to GAPDH ( n = 6). ∗ p

    Article Snippet: TGF-β 1 was purchased from PEPROTECH (100-21C).

    Techniques: Western Blot

    GW9662 counteracted puerarin's suppression effect on EndMT. (a) HUVECs were preincubated with puerarin (50 μ M) or pioglitazone (20 μ M) in the presence or absence of GW9662 (10 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. The protein levels of CD31, vimentin, p-Smad2, Smad2, Smad4, and PPAR- γ in cell lysates of indicated groups were detected by WB, normalized to GAPDH ( n = 6). ∗ p

    Journal: PPAR Research

    Article Title: Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition

    doi: 10.1155/2017/2647129

    Figure Lengend Snippet: GW9662 counteracted puerarin's suppression effect on EndMT. (a) HUVECs were preincubated with puerarin (50 μ M) or pioglitazone (20 μ M) in the presence or absence of GW9662 (10 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. The protein levels of CD31, vimentin, p-Smad2, Smad2, Smad4, and PPAR- γ in cell lysates of indicated groups were detected by WB, normalized to GAPDH ( n = 6). ∗ p

    Article Snippet: TGF-β 1 was purchased from PEPROTECH (100-21C).

    Techniques: Western Blot

    Puerarin inhibited TGF-β1-induced EndMT in HUVECs . (a–g) HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. mRNA levels of CD31, vimentin, α -SMA, collagen I, collagen III, CTGF, and Fn in indicated groups were tested by RT-PCR, normalized to GAPDH ( n = 6). ∗ p

    Journal: PPAR Research

    Article Title: Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition

    doi: 10.1155/2017/2647129

    Figure Lengend Snippet: Puerarin inhibited TGF-β1-induced EndMT in HUVECs . (a–g) HUVECs were preincubated with different concentrations of puerarin (10, 25, and 50 μ M) for 30 min and then treated with TGF- β 1 (10 ng/ml) for 48 h. mRNA levels of CD31, vimentin, α -SMA, collagen I, collagen III, CTGF, and Fn in indicated groups were tested by RT-PCR, normalized to GAPDH ( n = 6). ∗ p

    Article Snippet: TGF-β 1 was purchased from PEPROTECH (100-21C).

    Techniques: Reverse Transcription Polymerase Chain Reaction

    Pressure overload-induced cardiac fibrosis was alleviated in puerarin-treated mice . (a) Histological sections of the left ventricle in indicated groups were stained with PSR for fibrosis (upper and middle panel, scale bars: 100 μ m). α -SMA was detected with immunohistochemistry (lower panel, scale bars: 200 μ m). (b) TGF- β 1/Smad2 signaling pathway and α -SMA protein in indicated groups were determined by WB, normalized to GAPDH ( n = 6). ∗ p

    Journal: PPAR Research

    Article Title: Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-β1/Smad2-Mediated Endothelial-to-Mesenchymal Transition

    doi: 10.1155/2017/2647129

    Figure Lengend Snippet: Pressure overload-induced cardiac fibrosis was alleviated in puerarin-treated mice . (a) Histological sections of the left ventricle in indicated groups were stained with PSR for fibrosis (upper and middle panel, scale bars: 100 μ m). α -SMA was detected with immunohistochemistry (lower panel, scale bars: 200 μ m). (b) TGF- β 1/Smad2 signaling pathway and α -SMA protein in indicated groups were determined by WB, normalized to GAPDH ( n = 6). ∗ p

    Article Snippet: TGF-β 1 was purchased from PEPROTECH (100-21C).

    Techniques: Mouse Assay, Staining, Immunohistochemistry, Western Blot

    ALK4/5/7 inhibitor and TGF-β neutralizing antibodies, but not sActRIIB-Fc, effectively block SMAD2/3 signaling upon fluid flow stimulation. a ALK4/5/7 inhibitor (LY-364947; n = 3) significantly reduces baseline and fluid flow increased expression of Pai1, Fn1, Col1a1, Ptgs2, and Snai1 while the expression of Snai2 is less decreased. b TGF-β neutralizing antibodies (TGF-β Ab; n = 3) inhibited fluid flow-induced expression of SMAD2/3 target genes ( Pai1 and Fn1 ), while c soluble activin type-IIB-receptor fusion protein (sActRIIB-Fc; n = 5) did not. d Combining TGF-β Ab with sActRIIB-Fc ( n = 4) did not further increase the inhibitory effect. e TGF-β1 ( n = 2) or activin B ( n = 3) ligand-induced Pai1 expression was effectively inhibited by TGF-β Ab or sActRIIB-Fc, respectively ( t = 4 h). Parallel plate flow chamber induced fluid shear stress in PTECs at t = 16 h ( a – d ); qPCR, Hprt served as housekeeping gene to correct for cDNA input; data normalized to unstimulated controls (fold change); n = 2–5 per condition as indicated. * P

    Journal: Cellular and Molecular Life Sciences

    Article Title: Fluid shear stress-induced TGF-β/ALK5 signaling in renal epithelial cells is modulated by MEK1/2

    doi: 10.1007/s00018-017-2460-x

    Figure Lengend Snippet: ALK4/5/7 inhibitor and TGF-β neutralizing antibodies, but not sActRIIB-Fc, effectively block SMAD2/3 signaling upon fluid flow stimulation. a ALK4/5/7 inhibitor (LY-364947; n = 3) significantly reduces baseline and fluid flow increased expression of Pai1, Fn1, Col1a1, Ptgs2, and Snai1 while the expression of Snai2 is less decreased. b TGF-β neutralizing antibodies (TGF-β Ab; n = 3) inhibited fluid flow-induced expression of SMAD2/3 target genes ( Pai1 and Fn1 ), while c soluble activin type-IIB-receptor fusion protein (sActRIIB-Fc; n = 5) did not. d Combining TGF-β Ab with sActRIIB-Fc ( n = 4) did not further increase the inhibitory effect. e TGF-β1 ( n = 2) or activin B ( n = 3) ligand-induced Pai1 expression was effectively inhibited by TGF-β Ab or sActRIIB-Fc, respectively ( t = 4 h). Parallel plate flow chamber induced fluid shear stress in PTECs at t = 16 h ( a – d ); qPCR, Hprt served as housekeeping gene to correct for cDNA input; data normalized to unstimulated controls (fold change); n = 2–5 per condition as indicated. * P

    Article Snippet: Recombinant human TGF-β1 (#100-21) and recombinant human TGF-β2 (#100-35B) were purchased from PeproTech.

    Techniques: Blocking Assay, Flow Cytometry, Expressing, Real-time Polymerase Chain Reaction

    MEK inhibition modulates fluid shear-induced and TGF-β-stimulated expression of SMAD2/3 target genes. a MEK inhibition (Trametinib, GSK1120212) reduces TGF-β1 increased expression of Pai1, Fn1, Col1a1, Ptgs2, Snai1, and Vim , while expression of Cdh1 is less decreased. Snai2 expression was not significantly changed upon MEK inhibition. Relative mRNA expression measured at t = 4 h; n = 3; Hprt served as housekeeping gene to correct for cDNA input; data normalized to unstimulated controls. Significant difference ( P

    Journal: Cellular and Molecular Life Sciences

    Article Title: Fluid shear stress-induced TGF-β/ALK5 signaling in renal epithelial cells is modulated by MEK1/2

    doi: 10.1007/s00018-017-2460-x

    Figure Lengend Snippet: MEK inhibition modulates fluid shear-induced and TGF-β-stimulated expression of SMAD2/3 target genes. a MEK inhibition (Trametinib, GSK1120212) reduces TGF-β1 increased expression of Pai1, Fn1, Col1a1, Ptgs2, Snai1, and Vim , while expression of Cdh1 is less decreased. Snai2 expression was not significantly changed upon MEK inhibition. Relative mRNA expression measured at t = 4 h; n = 3; Hprt served as housekeeping gene to correct for cDNA input; data normalized to unstimulated controls. Significant difference ( P

    Article Snippet: Recombinant human TGF-β1 (#100-21) and recombinant human TGF-β2 (#100-35B) were purchased from PeproTech.

    Techniques: Inhibition, Expressing

    Dose- and time-dependent activation of SMAD2/3 signaling by TGF-β and activin. a Increased expression of Pai1, Fn1, Col1a1, Ptgs2, Snai1 , and Vim , and reduced expression of Snai2 and Cdh1 , upon stimulation with 5 ng/ml TGF-β1 ( n = 3, t = 4 h). b A dose response experiment shows increased sensitivity of Pai1 mRNA expression for TGF-β1 ( n = 4) compared to activin B ( n = 2) stimulation ( t = 4 h). c Pai1 expression shows stronger induction upon TGF-β1 or TGF-β2, compared to activin A or activin B ( n = 4 per condition, t = 4 h). d Time response (0–240 min) of target genes upon 5 ng/ml TGF-β1 stimulation ( n = 2). Expression was significantly different ( P

    Journal: Cellular and Molecular Life Sciences

    Article Title: Fluid shear stress-induced TGF-β/ALK5 signaling in renal epithelial cells is modulated by MEK1/2

    doi: 10.1007/s00018-017-2460-x

    Figure Lengend Snippet: Dose- and time-dependent activation of SMAD2/3 signaling by TGF-β and activin. a Increased expression of Pai1, Fn1, Col1a1, Ptgs2, Snai1 , and Vim , and reduced expression of Snai2 and Cdh1 , upon stimulation with 5 ng/ml TGF-β1 ( n = 3, t = 4 h). b A dose response experiment shows increased sensitivity of Pai1 mRNA expression for TGF-β1 ( n = 4) compared to activin B ( n = 2) stimulation ( t = 4 h). c Pai1 expression shows stronger induction upon TGF-β1 or TGF-β2, compared to activin A or activin B ( n = 4 per condition, t = 4 h). d Time response (0–240 min) of target genes upon 5 ng/ml TGF-β1 stimulation ( n = 2). Expression was significantly different ( P

    Article Snippet: Recombinant human TGF-β1 (#100-21) and recombinant human TGF-β2 (#100-35B) were purchased from PeproTech.

    Techniques: Activation Assay, Expressing

    3.1. Th17 and Th1 cells are found in the K/BxN arthritis model

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: 3.1. Th17 and Th1 cells are found in the K/BxN arthritis model

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques:

    Neutralizing anti-IFNγ antibody enhances Th17 induced arthritis. On day 0 of Th17 cell transfer mice were injected with 250 µg anti-IFNγ or control PIP antibody. Mice were injected every 10 days with antibody. a , The thickness

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: Neutralizing anti-IFNγ antibody enhances Th17 induced arthritis. On day 0 of Th17 cell transfer mice were injected with 250 µg anti-IFNγ or control PIP antibody. Mice were injected every 10 days with antibody. a , The thickness

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques: Mouse Assay, Injection

    Th17 and Th1 polarized KRN T cells transferred into B6.TCR.Cα −/− H-2 b/g7 mice induced arthritis. Naive KRN T cells were cultured for 3 weeks under Th17 or Th1 polarizing conditions using B6.G7 splenocytes as antigen presenting cells.

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: Th17 and Th1 polarized KRN T cells transferred into B6.TCR.Cα −/− H-2 b/g7 mice induced arthritis. Naive KRN T cells were cultured for 3 weeks under Th17 or Th1 polarizing conditions using B6.G7 splenocytes as antigen presenting cells.

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques: Mouse Assay, Cell Culture

    IgG 2b is the dominant anti-GPI isotype in mice transferred with Th17 polarized KRN T cells while IgG 1 is dominant in mice transferred with naive T cells and KRN/T-bet −/− Th17 cells. Serum titers of individual isotypes of anti-GPI were

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: IgG 2b is the dominant anti-GPI isotype in mice transferred with Th17 polarized KRN T cells while IgG 1 is dominant in mice transferred with naive T cells and KRN/T-bet −/− Th17 cells. Serum titers of individual isotypes of anti-GPI were

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques: Mouse Assay

    IFNγ is suppressed in Th17 polarized T cells from KRN/T-bet −/− mice in vitro but not in vivo. Naive KRN/T-bet −/− T cells were cultured for 3 weeks under Th17 polarizing conditions using B6.G7 splenocytes as antigen

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: IFNγ is suppressed in Th17 polarized T cells from KRN/T-bet −/− mice in vitro but not in vivo. Naive KRN/T-bet −/− T cells were cultured for 3 weeks under Th17 polarizing conditions using B6.G7 splenocytes as antigen

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques: Mouse Assay, In Vitro, In Vivo, Cell Culture

    Neutralizing anti-IL-17A antibody delayed Th17 induced arthritis. On day 0 of Th17 cell transfer mice were injected with 500 µg anti-IL-17A or control antibody. Mice were injected every 3 days with 250 µg antibody. a , The thickness of

    Journal: Journal of autoimmunity

    Article Title: Th17 cells can provide B cell help in autoantibody induced arthritis

    doi: 10.1016/j.jaut.2010.10.007

    Figure Lengend Snippet: Neutralizing anti-IL-17A antibody delayed Th17 induced arthritis. On day 0 of Th17 cell transfer mice were injected with 500 µg anti-IL-17A or control antibody. Mice were injected every 3 days with 250 µg antibody. a , The thickness of

    Article Snippet: Cells were cultured under Th1 conditions [5 U/ml recombinant murine IL-12 (Peprotech Inc., Rocky Hill, NJ), and 10% 11B11 supernatant containing anti-IL-4] or Th17 conditions [6 ng/ml recombinant human TGF-β1(Peprotech), 40 ng/ml recombinant murine IL-6 (Peprotech), 10 µg/ml hamster anti-murine IFNγ monoclonal antibody (kindly provided by R. Schreiber, Washington University), 10% Tosh supernatant containing anti-IL-12 and anti-IL-4] for 3 weeks.

    Techniques: Mouse Assay, Injection

    Effects of thalidomide (THD) on morphological transformation of myofibroblast (MF) induced by transforming growth factor (TGF)-β1. Human fetal lung fibroblast (HFL-F) were incubated for 4 days with 0·1% fetal bovine serum (a), TGF-β1

    Journal:

    Article Title: Thalidomide has a therapeutic effect on interstitial lung fibrosis: evidence from in vitro and in vivo studies

    doi: 10.1111/j.1365-2249.2009.03962.x

    Figure Lengend Snippet: Effects of thalidomide (THD) on morphological transformation of myofibroblast (MF) induced by transforming growth factor (TGF)-β1. Human fetal lung fibroblast (HFL-F) were incubated for 4 days with 0·1% fetal bovine serum (a), TGF-β1

    Article Snippet: Recombined human TGF-β1 was purchased from Peprotech (London, UK).

    Techniques: Transformation Assay, Incubation