recombinant murine il 17a  (PeproTech)

 
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    Name:
    Recombinant Murine IL 17 IL 17A
    Description:
    The originally described IL 17 protein now known as IL 17A is a disulfide linked homodimer secreted by activated T cells that act on stromal cells to induce production of proinflammatory and hematopoietic bioactive molecules Today IL 17 represents a family of structurally related cytokines that share a highly conserved C terminal region but differ from one another in their N terminal regions and in their distinct biological roles The six known members of this family IL 17A through IL 17F are secreted as homodimers IL 17A exhibits cross species bioactivity between human and murine cells Recombinant murine IL 17A is a 30 0 kDa disulfide linked homodimer of two 133 amino acid polypeptide chains
    Catalog Number:
    210-17-100UG
    Price:
    600.00
    Category:
    Recombinant Proteins
    Source:
    E.coli
    Reactivity:
    Rat
    Purity:
    98.0
    Quantity:
    100UG
    Buy from Supplier


    Structured Review

    PeproTech recombinant murine il 17a
    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant <t>IL-17A</t> or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    The originally described IL 17 protein now known as IL 17A is a disulfide linked homodimer secreted by activated T cells that act on stromal cells to induce production of proinflammatory and hematopoietic bioactive molecules Today IL 17 represents a family of structurally related cytokines that share a highly conserved C terminal region but differ from one another in their N terminal regions and in their distinct biological roles The six known members of this family IL 17A through IL 17F are secreted as homodimers IL 17A exhibits cross species bioactivity between human and murine cells Recombinant murine IL 17A is a 30 0 kDa disulfide linked homodimer of two 133 amino acid polypeptide chains
    https://www.bioz.com/result/recombinant murine il 17a/product/PeproTech
    Average 96 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    recombinant murine il 17a - by Bioz Stars, 2021-06
    96/100 stars

    Images

    1) Product Images from "Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells"

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2018.3600

    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    Figure Legend Snippet: Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Techniques Used: shRNA, Activation Assay, In Vitro, Infection, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Standard Deviation, Negative Control

    IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells
    Figure Legend Snippet: IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Techniques Used: Activation Assay, In Vitro, Recombinant, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Western Blot, Standard Deviation

    Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.
    Figure Legend Snippet: Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Techniques Used: Activation Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, shRNA, Negative Control

    2) Product Images from "Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6"

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    Journal: World Journal of Gastroenterology : WJG

    doi: 10.3748/wjg.v18.i28.3696

    Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P
    Figure Legend Snippet: Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P

    Techniques Used: shRNA, Transduction, Sequencing, Expressing, Infection, Polymerase Chain Reaction

    Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P
    Figure Legend Snippet: Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay

    Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P
    Figure Legend Snippet: Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P

    Techniques Used: shRNA, Expressing, Infection

    3) Product Images from "Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis"

    Article Title: Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis

    Journal: Oncotarget

    doi: 10.18632/oncotarget.20823

    IL-17A-promoted MSC2 polarization related with new bone formation of AS patients Values are the mean ± SEM. * P
    Figure Legend Snippet: IL-17A-promoted MSC2 polarization related with new bone formation of AS patients Values are the mean ± SEM. * P

    Techniques Used:

    IL-17A-promoted MSC2 polarization related with new bone formation of PGISp mice Values are the mean ± SEM (all n = 3). * P
    Figure Legend Snippet: IL-17A-promoted MSC2 polarization related with new bone formation of PGISp mice Values are the mean ± SEM (all n = 3). * P

    Techniques Used: Mouse Assay

    IL-17A-mediated MSC polarizations in AS Inflam: inflammation; NBF: new bone formation; H-IL17A: high level of IL-17A; L-IL17A: low level of IL-17A.
    Figure Legend Snippet: IL-17A-mediated MSC polarizations in AS Inflam: inflammation; NBF: new bone formation; H-IL17A: high level of IL-17A; L-IL17A: low level of IL-17A.

    Techniques Used:

    IL-17A mediated MSC1 and MSC2 polarizations in concentration-dependent way Values are the mean ± SEM (all n = 3). * P
    Figure Legend Snippet: IL-17A mediated MSC1 and MSC2 polarizations in concentration-dependent way Values are the mean ± SEM (all n = 3). * P

    Techniques Used: Concentration Assay

    4) Product Images from "Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells"

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2018.3600

    IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells
    Figure Legend Snippet: IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Techniques Used: Activation Assay, In Vitro, Recombinant, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Western Blot, Standard Deviation

    Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.
    Figure Legend Snippet: Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Techniques Used: Activation Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, shRNA, Negative Control

    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    Figure Legend Snippet: Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Techniques Used: shRNA, Activation Assay, In Vitro, Infection, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Standard Deviation, Negative Control

    Related Articles

    Concentration Assay:

    Article Title: Characterization and biological significance of IL-23-induced neutrophil polarization
    Article Snippet: .. Anti-β-actin mAb was purchased from Sigma-Aldrich and its working concentration (1:50 000) was determined in previous studies., Recombinant mouse cytokines were used at the following concentrations based on our previous studies: recombinant mouse IL-1β (100 ng/ml, PeproTech), IL-2 (10 ng/ml, PeproTech), IL-4 (10 ng/ml, R & D Systems), IL-6 (50 ng/ml, PeproTech), IL-10 (20 ng/ml, PeproTech), IL-12 (5 ng/ml, PeproTech), IL-13 (50 ng/ml, PeproTech), IL-17A (100 ng/ml, PeproTech), IL-21 (50 ng/ml, R & D Systems), IL-23 (10 ng/ml, R & D Systems), IL-33 (100 ng/ml, R & D Systems), LPS (1 μg/ml, Sigma-Aldrich), IFN-γ (100 ng/ml, PeproTech), TNF-α (100 ng/ml, PeproTech), TGF-β1 (5 ng/ml, R & D Systems), GM-CSF (40 ng/ml, R & D Systems) and G-CSF (100 ng/ml, Biovision, Milpitas, CA, USA). .. Tibiae and femora from BALB/c or B6 mice were removed using sterile techniques, and bone marrow was flushed with PBS.

    Recombinant:

    Article Title: Characterization and biological significance of IL-23-induced neutrophil polarization
    Article Snippet: .. Anti-β-actin mAb was purchased from Sigma-Aldrich and its working concentration (1:50 000) was determined in previous studies., Recombinant mouse cytokines were used at the following concentrations based on our previous studies: recombinant mouse IL-1β (100 ng/ml, PeproTech), IL-2 (10 ng/ml, PeproTech), IL-4 (10 ng/ml, R & D Systems), IL-6 (50 ng/ml, PeproTech), IL-10 (20 ng/ml, PeproTech), IL-12 (5 ng/ml, PeproTech), IL-13 (50 ng/ml, PeproTech), IL-17A (100 ng/ml, PeproTech), IL-21 (50 ng/ml, R & D Systems), IL-23 (10 ng/ml, R & D Systems), IL-33 (100 ng/ml, R & D Systems), LPS (1 μg/ml, Sigma-Aldrich), IFN-γ (100 ng/ml, PeproTech), TNF-α (100 ng/ml, PeproTech), TGF-β1 (5 ng/ml, R & D Systems), GM-CSF (40 ng/ml, R & D Systems) and G-CSF (100 ng/ml, Biovision, Milpitas, CA, USA). .. Tibiae and femora from BALB/c or B6 mice were removed using sterile techniques, and bone marrow was flushed with PBS.

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6
    Article Snippet: .. Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ). .. Anti-IL-17R (sc-1902, dilution factor 1:200) was purchased from Santa Cruz Biotechnology (Santa Cruz, CA).

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells
    Article Snippet: .. Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h. .. Total proteins were isolated from liver tissues and primary HSCs using radioimmunoprecipitation assay lysis buffer (P0013B), and protein concentration was quantified using a Bicinchoninic Acid Protein assay kit (P0009) (both from Beyotime Institute of Biotechnology, Shanghai, China).

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor
    Article Snippet: Twenty-five microliters of this antibody was combined in 6-mL polypropylene tubes with 25 μL of a 1 mg/mL suspension of streptavidin-coated paramagnetic beads (Dynal Inc., Lake Success, New York, USA) diluted in ECL buffer. .. Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added. ..

    Activation Assay:

    Article Title: Gene Expression Profiling of IL-17A-Treated Synovial Fibroblasts from the Human Temporomandibular Joint
    Article Snippet: Furthermore, PI3K/Akt promotes survival by inhibiting p53 and Bak/Bax-mediated apoptosis and triggering AP1 activation [ ]. .. We therefore suggest that IL-17A activates several signaling pathways other than the NFκ B activation pathway for IL-6 production in synovial fibroblasts ( ). .. In this study, our findings demonstrated that IL-17A upregulation of the expression of IL-6 and chemokines that is mediated by the NFκ B pathway is important in promoting leukocyte attraction to and invasion of the synovial tissue of TMD ( ).

    other:

    Article Title: Cytokine levels contribute to the pathogenesis of minimal hepatic encephalopathy in patients with hepatocellular carcinoma via STAT3 activation
    Article Snippet: We found that, in contrast to protein levels, levels of IL-17a and IFNλ3 mRNA were not associated with MHE (P = 0.211 and 0.530, respectively).

    In Vitro:

    Article Title: Chemoresistance of Human Monocyte-Derived Dendritic Cells Is Regulated by IL-17A
    Article Snippet: .. Here, we provide original evidence that the usual pattern of short-time (two days) DC lifespan is significantly extended beyond 12 days by exposure of DC to IL-17A, in vitro . .. Interestingly, the pro-inflammatory IL-17A up-regulates macrophage markers in DC and induces, via NF-κB, the expression of BCL2A1.

    Incubation:

    Article Title: Gene Expression Profiling of IL-17A-Treated Synovial Fibroblasts from the Human Temporomandibular Joint
    Article Snippet: Enzyme Linked Immunosorbent Assay (ELISA) Synovial fibroblasts were plated at a density of 5 × 104 cells per well in 24-well plates with Ham's F12 medium containing 10% FBS. .. After incubation with IL-17A for the appropriate length of time, culture supernatants were collected and stored at −80°C until use. .. The kinetics of IL-6 protein production was examined in control samples and in synovial fibroblasts incubated with IL-17A (10 ng/mL) for 4, 8, 12, and 24 h. To examine the dose dependency of IL-6 protein expression, the cells were treated with IL-17A at concentrations of 1, 10, and 50 ng/mL for 24 h. The IL-6 levels in the conditioned medium were measured using ELISA kit (R & D Systems, McKinley, MN, USA), according to the manufacturer's protocol.

    Infection:

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells
    Article Snippet: .. Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h. .. Total proteins were isolated from liver tissues and primary HSCs using radioimmunoprecipitation assay lysis buffer (P0013B), and protein concentration was quantified using a Bicinchoninic Acid Protein assay kit (P0009) (both from Beyotime Institute of Biotechnology, Shanghai, China).

    shRNA:

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells
    Article Snippet: .. Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h. .. Total proteins were isolated from liver tissues and primary HSCs using radioimmunoprecipitation assay lysis buffer (P0013B), and protein concentration was quantified using a Bicinchoninic Acid Protein assay kit (P0009) (both from Beyotime Institute of Biotechnology, Shanghai, China).

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  • 96
    PeproTech recombinant murine il 17a
    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant <t>IL-17A</t> or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.
    Recombinant Murine Il 17a, supplied by PeproTech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant murine il 17a/product/PeproTech
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    Price from $9.99 to $1999.99
    recombinant murine il 17a - by Bioz Stars, 2021-06
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    96
    PeproTech mouse recombinant il 17
    Apoptosis of blood Ly6G + CD11b + cells to <t>IL-17</t> and TLR2 ligand stimulation in the presence of GM-CSF. Representative density-plot histograms showing apoptosis of neutrophils from A) PBS and B) ZIA group. Blood neutrophils incubated in medium containing GM-CSF (50 ng/ml) were stimulated with zymosan (20 µg/ml) in the absence or presence of IL-17 (40 ng/ml) and cultured at 37°C, 5% CO 2 for 24 hours. Apoptosis was measured by Annexin V-PI staining kit and analysed by flow cytometry. C) Effect of IL-17 and TLR2 on the frequencies of Annexin V + Ly6G + cells in the GM-CSF loaded environment. Data represent the mean ± SEM of Annexin V + cells ( n = 5 animals per group in 3 experiments). * p
    Mouse Recombinant Il 17, supplied by PeproTech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Ad-ACVR2A shRNA suppresses IL-17-induced activation of primary mHSCs in vitro . The primary mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA for 24 h, and were then stimulated with recombinant IL-17A or IL-17F for an additional 48 h. (A) Knockdown efficiency of Ad-ACVR2A shRNA was confirmed in normal mHSCs by western blot analysis. (B and D) Production of collagens I and VI in cell supernatants were determined by ELISA kits. (C and E) Protein expression levels of α-SMA, p-Smad2 and total Smad2 were determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; ACVR2A, activin A receptor type 2A; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells; NC, negative control; p, phosphorylated; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: shRNA, Activation Assay, In Vitro, Infection, Recombinant, Western Blot, Enzyme-linked Immunosorbent Assay, Expressing, Standard Deviation, Negative Control

    IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: IL-17 induces activation of primary mHSCs in vitro . Recombinant mouse (A and B) IL-17A and (E and F) IL-17F (10, 30 or 100 ng/ml) were used to stimulate primary mHSCs for 48 h. In addition, mHSCs were treated with 30 ng/ml (C and D) IL-17A and (G and H) IL-17F for the indicated time periods. Activin A content in cell supernatants was determined by ELISA, and the expression levels of the marker for the activated HSCs, α-SMA, was determined by western blot analysis. Data are expressed as the means ± standard deviation (n=3/group). α-SMA, α-smooth muscle actin; IL-17, interleukin-17; mHSCs, mouse hepatic stellate cells

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, In Vitro, Recombinant, Enzyme-linked Immunosorbent Assay, Expressing, Marker, Western Blot, Standard Deviation

    Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Journal: International Journal of Molecular Medicine

    Article Title: Adenovirus-mediated knockdown of activin A receptor type 2A attenuates immune-induced hepatic fibrosis in mice and inhibits interleukin-17-induced activation of primary hepatic stellate cells

    doi: 10.3892/ijmm.2018.3600

    Figure Lengend Snippet: Chronic treatment with Con A induces activation of activin and IL-17 signaling in mouse liver. (A) Experiment part 1: Mice were administered Con A (8 mg/kg/week) for up to 6 weeks, in order to generate a model of immune-associated liver fibrosis. (B–E) Serum and liver levels of activin A, IL-17A and IL-17F were detected in mice in the control and Con A groups using specific ELISA kits. (F) mRNA and (G) protein expression levels of ACVR2A were determined using reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Data are expressed as the means ± standard deviation. (H) Experiment part 2: Mice in the Con A groups were administered two injections of Ad-ACVR2A shRNA or Ad-NC shRNA at the indicated timepoints. (I–K) Protein expression levels of ACVR2A were analyzed in mouse liver tissues collected from the various groups. Data are expressed as the means ± standard error. ACVR2A, activin A receptor type 2A; Con A, concanavalin A; IL-17, interleukin-17; NC, negative control; shRNA, short hairpin RNA.

    Article Snippet: Recombinant murine IL-17A and IL-17F (PeproTech, Inc., Rocky Hill, NJ, USA) at 10, 30 or 100 ng/ml were used to stimulate mHSCs for 1, 3, 6, 12, 24 or 48 h. For some experiments, the mHSCs were infected with Ad-ACVR2A shRNA or Ad-NC shRNA (multiplicity of infection, both 50) for 24 h, and were then stimulated with recombinant IL-17A (30 ng/ml) or IL-17F (30 ng/ml) for additional 48 h.

    Techniques: Activation Assay, Mouse Assay, Enzyme-linked Immunosorbent Assay, Expressing, Real-time Polymerase Chain Reaction, Western Blot, Standard Deviation, shRNA, Negative Control

    Release of IL-18 in splenocytes from ICE KO mice. Splenocytes from WT or ICE KO mice were cultured for 24 hours in the absence of any exogenous stimulation. IL-18 levels were measured in supernatants. Data are mean ± SEM of 8 mice per group. ** P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Release of IL-18 in splenocytes from ICE KO mice. Splenocytes from WT or ICE KO mice were cultured for 24 hours in the absence of any exogenous stimulation. IL-18 levels were measured in supernatants. Data are mean ± SEM of 8 mice per group. ** P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Mouse Assay, Cell Culture

    Constitutive expression of pro–IL-18 in the spleens and livers on untreated mice. Spleen and liver homogenates from 3 untreated mice were subjected to Western blot analysis with a specific rabbit anti-murine IL-18 antiserum. Recombinant murine pro–IL-18 and mature IL-18 were used as standards.

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Constitutive expression of pro–IL-18 in the spleens and livers on untreated mice. Spleen and liver homogenates from 3 untreated mice were subjected to Western blot analysis with a specific rabbit anti-murine IL-18 antiserum. Recombinant murine pro–IL-18 and mature IL-18 were used as standards.

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Expressing, Mouse Assay, Western Blot, Recombinant

    Increase in serum IL-18 levels after IL-12 administration. WT and ICE KO mice received 4 daily intraperitoneal injections of IL-12 (100 or 400 ng/mouse) or vehicle. Two hours after the fourth injection, blood was collected and serum was prepared. Data are mean ± SEM of 10 mice per group. * P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Increase in serum IL-18 levels after IL-12 administration. WT and ICE KO mice received 4 daily intraperitoneal injections of IL-12 (100 or 400 ng/mouse) or vehicle. Two hours after the fourth injection, blood was collected and serum was prepared. Data are mean ± SEM of 10 mice per group. * P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Mouse Assay, Injection

    Neutralization of IL-18 reduces IL-12–induced IFN-γ levels in vivo. Mice received 4 daily intraperitoneal injections of IL-12 (100 ng/mouse). One hour before the first and the third injection, the antibody-treated group received an intraperitoneal injection of 200 μL of rabbit anti–IL-18 antiserum, whereas the control group received the same amount of NRS. Two hours after the fourth injection, blood was collected and serum was prepared for measurement of IFN-γ. Data are mean ± SEM of 5 mice per group. ** P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Neutralization of IL-18 reduces IL-12–induced IFN-γ levels in vivo. Mice received 4 daily intraperitoneal injections of IL-12 (100 ng/mouse). One hour before the first and the third injection, the antibody-treated group received an intraperitoneal injection of 200 μL of rabbit anti–IL-18 antiserum, whereas the control group received the same amount of NRS. Two hours after the fourth injection, blood was collected and serum was prepared for measurement of IFN-γ. Data are mean ± SEM of 5 mice per group. ** P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Neutralization, In Vivo, Mouse Assay, Injection

    IL-18 production in unstimulated and IL-12–stimulated splenocytes. Splenocytes were cultured in RPMI-FBS for increasing amounts of time without added exogenous stimulation, or with IL-12 at 10 ng/mL. Cell-associated and released IL-18 levels were measured. Data are mean ± SEM of 9 mice per group.

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: IL-18 production in unstimulated and IL-12–stimulated splenocytes. Splenocytes were cultured in RPMI-FBS for increasing amounts of time without added exogenous stimulation, or with IL-12 at 10 ng/mL. Cell-associated and released IL-18 levels were measured. Data are mean ± SEM of 9 mice per group.

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

    Techniques: Cell Culture, Mouse Assay

    Effect of IL-18 neutralization on the induction of IFN-γ by IL-12 in vitro. Splenocytes were cultured for 48 hours with increasing concentrations of IL-12 (0.1–10 ng/mL) in the presence or absence of either neutralizing anti–IL-18 IgG or control IgG (50 μg/mL). IFN-γ levels were measured in the supernatants. Data are mean ± SEM of 3 mice per group and are representative of 1 experiment out of 3 performed. * P

    Journal: Journal of Clinical Investigation

    Article Title: IL-12-induced IFN-? is dependent on caspase-1 processing of the IL-18 precursor

    doi:

    Figure Lengend Snippet: Effect of IL-18 neutralization on the induction of IFN-γ by IL-12 in vitro. Splenocytes were cultured for 48 hours with increasing concentrations of IL-12 (0.1–10 ng/mL) in the presence or absence of either neutralizing anti–IL-18 IgG or control IgG (50 μg/mL). IFN-γ levels were measured in the supernatants. Data are mean ± SEM of 3 mice per group and are representative of 1 experiment out of 3 performed. * P

    Article Snippet: Tubes were shaken for 15 minutes at room temperature, after which 25 μL of samples or standard concentrations of recombinant murine IL-18 (PeproTech Inc., Rocky Hill, New Jersey, USA) was added.

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

    Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Short hairpin RNA design, interference efficiency assay, and lentivirus transduction. A: DNA sequence analysis of pGCSIL/Interleukin-17A receptor (IL-17RA) short hairpin RNA (shRNA) 1; B: Lentiviral-mediated IL-17RA shRNA 1, 2, 3, and 4 (shRNA 1, 2, 3, and 4) inhibited IL-17RA mRNA expression in hepatic stellate cells (HSCs). HSCs infected with lentivirus at a multiplicity of infection of 10 for 72 h, and IL-17RA mRNA expression was quantified by polymerase chain reaction. IL-17RA shRNA 1 was the most efficient silencing tool for IL-17RA. b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: shRNA, Transduction, Sequencing, Expressing, Infection, Polymerase Chain Reaction

    Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Mitogen activated protein kinases pathway involved in interleukin 17A induced interleukin 6 expression. A: Secretion of interleukin (IL)-6 in hepatic stellate cells (HSCs) induced by interleukin 17A (IL-17A) was determined using enzyme-linked immunosorbent assay. b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay

    Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P

    Journal: World Journal of Gastroenterology : WJG

    Article Title: Lentiviral vector-mediated down-regulation of IL-17A receptor in hepatic stellate cells results in decreased secretion of IL-6

    doi: 10.3748/wjg.v18.i28.3696

    Figure Lengend Snippet: Lentiviral-mediated interleukin 17A receptor short hairpin RNA arrested interleukin 6 expression, partly through suppressing phosphorylation of p38 mitogen activated protein kinases and extracellular regulated protein kinases 1/2. A: Lentiviral-mediated interleukin (IL)-17A receptor short hairpin RNA (shRNA) 1 [at multiplicity of infection (MOI) = 10 for 72 h] inhibited the expression of IL-17RA in hepatic stellate cells (HSCs); B: Lentiviral-mediated IL-17RA shRNA 1 inhibited IL-17A-induced IL-6 mRNA expression in HSCs. HSCs were infected with IL-17RA shRNA 1 or random shRNA lentivirus at MOI = 10 for 72 h, and followed by 3 h exposure to IL-17A (100 ng/mL). b P

    Article Snippet: Recombinant murine IL-17A was purchased from Peprothech (Princeton Business Park, NJ).

    Techniques: shRNA, Expressing, Infection

    Apoptosis of blood Ly6G + CD11b + cells to IL-17 and TLR2 ligand stimulation in the presence of GM-CSF. Representative density-plot histograms showing apoptosis of neutrophils from A) PBS and B) ZIA group. Blood neutrophils incubated in medium containing GM-CSF (50 ng/ml) were stimulated with zymosan (20 µg/ml) in the absence or presence of IL-17 (40 ng/ml) and cultured at 37°C, 5% CO 2 for 24 hours. Apoptosis was measured by Annexin V-PI staining kit and analysed by flow cytometry. C) Effect of IL-17 and TLR2 on the frequencies of Annexin V + Ly6G + cells in the GM-CSF loaded environment. Data represent the mean ± SEM of Annexin V + cells ( n = 5 animals per group in 3 experiments). * p

    Journal: Central-European Journal of Immunology

    Article Title: The effect of interleukin 17 and Toll-like receptor 2 on CD11b expression and apoptosis of neutrophils in zymosaninduced arthritis and paw oedema

    doi: 10.5114/ceji.2014.43712

    Figure Lengend Snippet: Apoptosis of blood Ly6G + CD11b + cells to IL-17 and TLR2 ligand stimulation in the presence of GM-CSF. Representative density-plot histograms showing apoptosis of neutrophils from A) PBS and B) ZIA group. Blood neutrophils incubated in medium containing GM-CSF (50 ng/ml) were stimulated with zymosan (20 µg/ml) in the absence or presence of IL-17 (40 ng/ml) and cultured at 37°C, 5% CO 2 for 24 hours. Apoptosis was measured by Annexin V-PI staining kit and analysed by flow cytometry. C) Effect of IL-17 and TLR2 on the frequencies of Annexin V + Ly6G + cells in the GM-CSF loaded environment. Data represent the mean ± SEM of Annexin V + cells ( n = 5 animals per group in 3 experiments). * p

    Article Snippet: Interleukin 17 administration in zymosaninduced paw oedema Female BALB/c mice were injected intra-peritoneally (i.p.) with mouse recombinant IL-17 (PeproTech EC, London, UK; 0.5 µg/200 µl/mice) or endotoxin free PBS (Bio-Wittaker® , Lonza; 200 µl) one hour before the induction of paw oedema.

    Techniques: Incubation, Cell Culture, Staining, Flow Cytometry, Cytometry

    Effect of IL-17 and TLR2 stimulation on the dynamic of Ly6G + cell apoptosis. Apoptosis of purified blood Ly6G + CD11b + cells from A) PBS group and B) ZIA group during culture period of 12 hours, 37°C, 5% CO 2 measured by commercial Annexin V kit. Neutrophils were stimulated with zymosan (20 µg/ml) in the presence or the absence of IL-17 (40 ng/ml). Apoptosis was evaluated at each time point in 6 samples per group and the values represent the mean ± SEM of Annexin V + neutrophils. ** p

    Journal: Central-European Journal of Immunology

    Article Title: The effect of interleukin 17 and Toll-like receptor 2 on CD11b expression and apoptosis of neutrophils in zymosaninduced arthritis and paw oedema

    doi: 10.5114/ceji.2014.43712

    Figure Lengend Snippet: Effect of IL-17 and TLR2 stimulation on the dynamic of Ly6G + cell apoptosis. Apoptosis of purified blood Ly6G + CD11b + cells from A) PBS group and B) ZIA group during culture period of 12 hours, 37°C, 5% CO 2 measured by commercial Annexin V kit. Neutrophils were stimulated with zymosan (20 µg/ml) in the presence or the absence of IL-17 (40 ng/ml). Apoptosis was evaluated at each time point in 6 samples per group and the values represent the mean ± SEM of Annexin V + neutrophils. ** p

    Article Snippet: Interleukin 17 administration in zymosaninduced paw oedema Female BALB/c mice were injected intra-peritoneally (i.p.) with mouse recombinant IL-17 (PeproTech EC, London, UK; 0.5 µg/200 µl/mice) or endotoxin free PBS (Bio-Wittaker® , Lonza; 200 µl) one hour before the induction of paw oedema.

    Techniques: Purification

    Administration of IL-17 in zymosan-induced paw oedema. A) Schedule of IL-17 treatment and the induction of paw inflammation. BALB/c mice were i.p. injected with IL-17 or PBS. After 30 minutes they received a sub-plantar injection of 30 µl zymosan suspension (20 mg/ml) at the hind paw and PBS at the contralateral one. B) Paw thickness measured in the medial-lateral direction at different time points post-zymosan injection using a calliper. The results are expressed as the difference (D) in mm between baseline and measurements after zymosan/PBS injection. Each time point represents the mean ± SEM ( n = 7 animals per group in 3 experiments), ANOVA. C) Ly6G + CD11b + cells in whole blood and D) expression of CD11b on Annexin V − neutrophils detected by flow cytometry. E) The frequencies of Annexin V + Ly6G + cells in blood and the amounts of GM-CSF in serum 4 hours after the induction of ZIO. Values in C, D, E and F are the mean ± SEM ( n = 7 animals per group in 3 experiments). * p

    Journal: Central-European Journal of Immunology

    Article Title: The effect of interleukin 17 and Toll-like receptor 2 on CD11b expression and apoptosis of neutrophils in zymosaninduced arthritis and paw oedema

    doi: 10.5114/ceji.2014.43712

    Figure Lengend Snippet: Administration of IL-17 in zymosan-induced paw oedema. A) Schedule of IL-17 treatment and the induction of paw inflammation. BALB/c mice were i.p. injected with IL-17 or PBS. After 30 minutes they received a sub-plantar injection of 30 µl zymosan suspension (20 mg/ml) at the hind paw and PBS at the contralateral one. B) Paw thickness measured in the medial-lateral direction at different time points post-zymosan injection using a calliper. The results are expressed as the difference (D) in mm between baseline and measurements after zymosan/PBS injection. Each time point represents the mean ± SEM ( n = 7 animals per group in 3 experiments), ANOVA. C) Ly6G + CD11b + cells in whole blood and D) expression of CD11b on Annexin V − neutrophils detected by flow cytometry. E) The frequencies of Annexin V + Ly6G + cells in blood and the amounts of GM-CSF in serum 4 hours after the induction of ZIO. Values in C, D, E and F are the mean ± SEM ( n = 7 animals per group in 3 experiments). * p

    Article Snippet: Interleukin 17 administration in zymosaninduced paw oedema Female BALB/c mice were injected intra-peritoneally (i.p.) with mouse recombinant IL-17 (PeproTech EC, London, UK; 0.5 µg/200 µl/mice) or endotoxin free PBS (Bio-Wittaker® , Lonza; 200 µl) one hour before the induction of paw oedema.

    Techniques: Mouse Assay, Injection, Expressing, Flow Cytometry, Cytometry