anti trpv4 antibody  (Alomone Labs)


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    Alomone Labs anti trpv4 antibody
    <t>TRPV4-mediated</t> Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P
    Anti Trpv4 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti trpv4 antibody/product/Alomone Labs
    Average 93 stars, based on 4 article reviews
    Price from $9.99 to $1999.99
    anti trpv4 antibody - by Bioz Stars, 2022-12
    93/100 stars

    Images

    1) Product Images from "Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis"

    Article Title: Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis

    Journal: Stem cells (Dayton, Ohio)

    doi: 10.1002/stem.3440

    TRPV4-mediated Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P
    Figure Legend Snippet: TRPV4-mediated Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P

    Techniques Used: Derivative Assay

    Trpv4 expression within chondrogenic cell population identified by Col2a1-GFP reporter. Induced pluripotent stem cells (iPSCs) underwent chondrogenesis for 15 days and were sorted into GFP+ and GFP− populations based on a Col2a1-GFP reporter before quantitative reverse transcription polymerase chain reaction (qRT-PCR) gene expression analysis for pluripotency gene Nanog , chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Controls: undifferentiated iPSCs and isolated primary murine articular chondrocytes (AC). Mean ± SEM, n = 5, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P
    Figure Legend Snippet: Trpv4 expression within chondrogenic cell population identified by Col2a1-GFP reporter. Induced pluripotent stem cells (iPSCs) underwent chondrogenesis for 15 days and were sorted into GFP+ and GFP− populations based on a Col2a1-GFP reporter before quantitative reverse transcription polymerase chain reaction (qRT-PCR) gene expression analysis for pluripotency gene Nanog , chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Controls: undifferentiated iPSCs and isolated primary murine articular chondrocytes (AC). Mean ± SEM, n = 5, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Techniques Used: Expressing, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Isolation

    Cell proliferation, sulfated glycosaminoglycan (sGAG) production, and chondrogenic gene expression in induced pluripotent stem cell (iPSC)-derived chondroprogenitors after transient activation of TRPV4. A, GFP+ and GFP− cells were formed into micromasses and underwent chondrogenesis for 7 days before being treated with GSK1016790A (GSK101) or GSK101+GSK205 for 1 hour per day, in the absence of chondrogenic growth factors. B, Day 21 biochemical analysis for DNA, sGAG, and collagen content showed that activation of TRPV4 with GSK101 increased DNA content, sGAG/DNA ratio in GFP+ groups only. Total collagen/DNA was not affected. C, Quantitative reverse transcription polymerase chain reaction (qRT-PCR) at day 21 showed significantly increased Sox9 and Acan expression in GFP+ cells in response to GSK101 treatment compared to controls conditions. Col2a1 expression was not significantly altered in either cell population in response to TRPV4 activation. Mean ± SEM, n = 5-6 for qPCR, n = 5 for biochemical measurements, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P
    Figure Legend Snippet: Cell proliferation, sulfated glycosaminoglycan (sGAG) production, and chondrogenic gene expression in induced pluripotent stem cell (iPSC)-derived chondroprogenitors after transient activation of TRPV4. A, GFP+ and GFP− cells were formed into micromasses and underwent chondrogenesis for 7 days before being treated with GSK1016790A (GSK101) or GSK101+GSK205 for 1 hour per day, in the absence of chondrogenic growth factors. B, Day 21 biochemical analysis for DNA, sGAG, and collagen content showed that activation of TRPV4 with GSK101 increased DNA content, sGAG/DNA ratio in GFP+ groups only. Total collagen/DNA was not affected. C, Quantitative reverse transcription polymerase chain reaction (qRT-PCR) at day 21 showed significantly increased Sox9 and Acan expression in GFP+ cells in response to GSK101 treatment compared to controls conditions. Col2a1 expression was not significantly altered in either cell population in response to TRPV4 activation. Mean ± SEM, n = 5-6 for qPCR, n = 5 for biochemical measurements, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Techniques Used: Expressing, Derivative Assay, Activation Assay, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

    Trpv4 expression during chondrogenesis of induced pluripotent stem cells (iPSCs). A, Alcian blue staining of iPSCs undergoing chondrogenic differentiation over 21 days. B, Gene expression for pluripotency genes Nanog and Sox2 , mesenchymal marker Vim , and chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Mean ± SEM, n = 5 per group, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P
    Figure Legend Snippet: Trpv4 expression during chondrogenesis of induced pluripotent stem cells (iPSCs). A, Alcian blue staining of iPSCs undergoing chondrogenic differentiation over 21 days. B, Gene expression for pluripotency genes Nanog and Sox2 , mesenchymal marker Vim , and chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Mean ± SEM, n = 5 per group, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Techniques Used: Expressing, Staining, Marker

    2) Product Images from "TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching"

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1901033

    p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p
    Figure Legend Snippet: p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p

    Techniques Used: Activation Assay, Inhibition

    TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p
    Figure Legend Snippet: TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p

    Techniques Used: Incubation

    TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p
    Figure Legend Snippet: TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p

    Techniques Used: Mouse Assay

    p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p
    Figure Legend Snippet: p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p

    Techniques Used: Incubation, Cell Culture

    TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p
    Figure Legend Snippet: TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p

    Techniques Used: Derivative Assay, Incubation

    TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p
    Figure Legend Snippet: TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p

    Techniques Used: Mouse Assay, Immunofluorescence

    TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p
    Figure Legend Snippet: TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p

    Techniques Used: Incubation, Cell Culture, Enzyme-linked Immunosorbent Assay

    3) Product Images from "TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching"

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1901033

    p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p
    Figure Legend Snippet: p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p

    Techniques Used: Activation Assay, Inhibition

    TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p
    Figure Legend Snippet: TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p

    Techniques Used: Incubation

    TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p
    Figure Legend Snippet: TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p

    Techniques Used: Mouse Assay

    p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p
    Figure Legend Snippet: p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p

    Techniques Used: Incubation, Cell Culture

    TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p
    Figure Legend Snippet: TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p

    Techniques Used: Derivative Assay, Incubation

    TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p
    Figure Legend Snippet: TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p

    Techniques Used: Mouse Assay, Immunofluorescence

    TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p
    Figure Legend Snippet: TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p

    Techniques Used: Incubation, Cell Culture, Enzyme-linked Immunosorbent Assay

    4) Product Images from "Rhythmic Calcium Events in the Lamina Propria Network of the Urinary Bladder of Rat Pups"

    Article Title: Rhythmic Calcium Events in the Lamina Propria Network of the Urinary Bladder of Rat Pups

    Journal: Frontiers in Systems Neuroscience

    doi: 10.3389/fnsys.2017.00087

    Whole mounts of urinary bladder tissue were prepared at the urothelial-lamina junction and contained a dense network of capillaries, small blood vessels and cells from rat pups aged ≤ P21. Capillaries, blood vessels and cells were loaded with the fluorescent dye (Fluo-2, green) (A , B,E) . Tetramethylrhodamine (TRITC; red) was picked up by urothelial cells and provided contrast to Fluo-2 loaded cells (A , B) . The cellular network in the lamina propria was heterogeneous with numerous small round, stellate or spindle shaped cells (10–20 μm) with multiple processes projecting from the soma in rat pups aged P ≤ 21. Numerous cells in the lamina propria exhibited PDGFRα-immunoreactivity (IR) whereas fewer cells exhibited TRPV4-IR (C,D) . At the urothelial-lamina propria junction, a dense capillary network was in close proximity to the network of cells expressing PDGFRα- and TRPV4-IR (E) . Capillaries were isolated using their signature, long tubular shape in the PTCL analysis software and recolored red to distinguish them from lamina propria cells. 3-D images of the capillary network and the lamina propria cell network at different angles of rotation (E , i , ii) . Calibration bar in (B) represents 10 μm (A , B) , 15 μm (C , D) . Calibration bar in (E) represents 5 μm.
    Figure Legend Snippet: Whole mounts of urinary bladder tissue were prepared at the urothelial-lamina junction and contained a dense network of capillaries, small blood vessels and cells from rat pups aged ≤ P21. Capillaries, blood vessels and cells were loaded with the fluorescent dye (Fluo-2, green) (A , B,E) . Tetramethylrhodamine (TRITC; red) was picked up by urothelial cells and provided contrast to Fluo-2 loaded cells (A , B) . The cellular network in the lamina propria was heterogeneous with numerous small round, stellate or spindle shaped cells (10–20 μm) with multiple processes projecting from the soma in rat pups aged P ≤ 21. Numerous cells in the lamina propria exhibited PDGFRα-immunoreactivity (IR) whereas fewer cells exhibited TRPV4-IR (C,D) . At the urothelial-lamina propria junction, a dense capillary network was in close proximity to the network of cells expressing PDGFRα- and TRPV4-IR (E) . Capillaries were isolated using their signature, long tubular shape in the PTCL analysis software and recolored red to distinguish them from lamina propria cells. 3-D images of the capillary network and the lamina propria cell network at different angles of rotation (E , i , ii) . Calibration bar in (B) represents 10 μm (A , B) , 15 μm (C , D) . Calibration bar in (E) represents 5 μm.

    Techniques Used: Expressing, Isolation, Software

    5) Product Images from "TRPV4 Mechanosensitive Ion Channel Regulates LPS-Stimulated Macrophage Phagocytosis"

    Article Title: TRPV4 Mechanosensitive Ion Channel Regulates LPS-Stimulated Macrophage Phagocytosis

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    doi: 10.4049/jimmunol.1501688

    TRPV4 modulates the cytokine response to LPS in a manner that depends on matrix stiffness
    Figure Legend Snippet: TRPV4 modulates the cytokine response to LPS in a manner that depends on matrix stiffness

    Techniques Used:

    Working model illustrating that LPS and TRPV4 signal cooperate to alter macrophage phenotypic change leading to enhanced clearance of infection and resolution of lung injury
    Figure Legend Snippet: Working model illustrating that LPS and TRPV4 signal cooperate to alter macrophage phenotypic change leading to enhanced clearance of infection and resolution of lung injury

    Techniques Used: Infection

    TRPV4 mediates LPS-stimulated macrophage phagocytosis of E. coli particles
    Figure Legend Snippet: TRPV4 mediates LPS-stimulated macrophage phagocytosis of E. coli particles

    Techniques Used:

    TRPV4 mediates LPS-stimulated macrophage phagocytosis of IgG-coated latex beads in vitro
    Figure Legend Snippet: TRPV4 mediates LPS-stimulated macrophage phagocytosis of IgG-coated latex beads in vitro

    Techniques Used: In Vitro

    TRPV4 mediates the stiffness induction effect on LPS-stimulated calcium influx and macrophage phagocytosis
    Figure Legend Snippet: TRPV4 mediates the stiffness induction effect on LPS-stimulated calcium influx and macrophage phagocytosis

    Techniques Used:

    TRPV4 mediates LPS-stimulated macrophage phagocytosis of IgG-coated latex beads in vivo
    Figure Legend Snippet: TRPV4 mediates LPS-stimulated macrophage phagocytosis of IgG-coated latex beads in vivo

    Techniques Used: In Vivo

    Functional TRPV4 is expressed in murine BMDMs
    Figure Legend Snippet: Functional TRPV4 is expressed in murine BMDMs

    Techniques Used: Functional Assay

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    Alomone Labs anti trpv4 antibody
    <t>TRPV4-mediated</t> Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P
    Anti Trpv4 Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti trpv4 antibody/product/Alomone Labs
    Average 93 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    anti trpv4 antibody - by Bioz Stars, 2022-12
    93/100 stars
      Buy from Supplier

    94
    Alomone Labs antibodies against trpv4
    Transwell assays demonstrated that <t>TRPV4</t> down-regulation greatly inhibited invasion abilities of gastric cancer cells. ( A and B ) Representative images of invasive cells following transfection with shTRPV4 or shCtrl. Magnification, ×200. ( C and D ) The column diagram of the numbers of invasive cells following transfection with shTRPV4 or shCtrl. **P
    Antibodies Against Trpv4, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against trpv4/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    antibodies against trpv4 - by Bioz Stars, 2022-12
    94/100 stars
      Buy from Supplier

    Image Search Results


    TRPV4-mediated Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P

    Journal: Stem cells (Dayton, Ohio)

    Article Title: Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis

    doi: 10.1002/stem.3440

    Figure Lengend Snippet: TRPV4-mediated Ca 2+ signaling. A, GFP-sorted induced pluripotent stem cell (iPSC)-derived chondroprogenitor cell response to TRPV4-mediated Ca 2+ signaling with GSK1016790A (GSK101) treatment measured by confocal cell traces, as compared to undifferentiated iPSCs or primary murine articular chondrocytes (AC) (N = 3 experiments, n = 78-161 cell traces per group; groups not sharing the same letter are statistically different from one another by Chi-square test, P

    Article Snippet: After sorting, cells were lysed for RNA isolation and subsequent qRT-PCR to measure expression of Nanog, Sox9, Acan, Col2a1 , and Trpv4 as described above, or seeded on gelatin-coated coverslips for 48 hours for TRPV4 immunocytochemistry.

    Techniques: Derivative Assay

    Trpv4 expression within chondrogenic cell population identified by Col2a1-GFP reporter. Induced pluripotent stem cells (iPSCs) underwent chondrogenesis for 15 days and were sorted into GFP+ and GFP− populations based on a Col2a1-GFP reporter before quantitative reverse transcription polymerase chain reaction (qRT-PCR) gene expression analysis for pluripotency gene Nanog , chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Controls: undifferentiated iPSCs and isolated primary murine articular chondrocytes (AC). Mean ± SEM, n = 5, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Journal: Stem cells (Dayton, Ohio)

    Article Title: Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis

    doi: 10.1002/stem.3440

    Figure Lengend Snippet: Trpv4 expression within chondrogenic cell population identified by Col2a1-GFP reporter. Induced pluripotent stem cells (iPSCs) underwent chondrogenesis for 15 days and were sorted into GFP+ and GFP− populations based on a Col2a1-GFP reporter before quantitative reverse transcription polymerase chain reaction (qRT-PCR) gene expression analysis for pluripotency gene Nanog , chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Controls: undifferentiated iPSCs and isolated primary murine articular chondrocytes (AC). Mean ± SEM, n = 5, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Article Snippet: After sorting, cells were lysed for RNA isolation and subsequent qRT-PCR to measure expression of Nanog, Sox9, Acan, Col2a1 , and Trpv4 as described above, or seeded on gelatin-coated coverslips for 48 hours for TRPV4 immunocytochemistry.

    Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Isolation

    Cell proliferation, sulfated glycosaminoglycan (sGAG) production, and chondrogenic gene expression in induced pluripotent stem cell (iPSC)-derived chondroprogenitors after transient activation of TRPV4. A, GFP+ and GFP− cells were formed into micromasses and underwent chondrogenesis for 7 days before being treated with GSK1016790A (GSK101) or GSK101+GSK205 for 1 hour per day, in the absence of chondrogenic growth factors. B, Day 21 biochemical analysis for DNA, sGAG, and collagen content showed that activation of TRPV4 with GSK101 increased DNA content, sGAG/DNA ratio in GFP+ groups only. Total collagen/DNA was not affected. C, Quantitative reverse transcription polymerase chain reaction (qRT-PCR) at day 21 showed significantly increased Sox9 and Acan expression in GFP+ cells in response to GSK101 treatment compared to controls conditions. Col2a1 expression was not significantly altered in either cell population in response to TRPV4 activation. Mean ± SEM, n = 5-6 for qPCR, n = 5 for biochemical measurements, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Journal: Stem cells (Dayton, Ohio)

    Article Title: Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis

    doi: 10.1002/stem.3440

    Figure Lengend Snippet: Cell proliferation, sulfated glycosaminoglycan (sGAG) production, and chondrogenic gene expression in induced pluripotent stem cell (iPSC)-derived chondroprogenitors after transient activation of TRPV4. A, GFP+ and GFP− cells were formed into micromasses and underwent chondrogenesis for 7 days before being treated with GSK1016790A (GSK101) or GSK101+GSK205 for 1 hour per day, in the absence of chondrogenic growth factors. B, Day 21 biochemical analysis for DNA, sGAG, and collagen content showed that activation of TRPV4 with GSK101 increased DNA content, sGAG/DNA ratio in GFP+ groups only. Total collagen/DNA was not affected. C, Quantitative reverse transcription polymerase chain reaction (qRT-PCR) at day 21 showed significantly increased Sox9 and Acan expression in GFP+ cells in response to GSK101 treatment compared to controls conditions. Col2a1 expression was not significantly altered in either cell population in response to TRPV4 activation. Mean ± SEM, n = 5-6 for qPCR, n = 5 for biochemical measurements, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Article Snippet: After sorting, cells were lysed for RNA isolation and subsequent qRT-PCR to measure expression of Nanog, Sox9, Acan, Col2a1 , and Trpv4 as described above, or seeded on gelatin-coated coverslips for 48 hours for TRPV4 immunocytochemistry.

    Techniques: Expressing, Derivative Assay, Activation Assay, Reverse Transcription Polymerase Chain Reaction, Quantitative RT-PCR, Real-time Polymerase Chain Reaction

    Trpv4 expression during chondrogenesis of induced pluripotent stem cells (iPSCs). A, Alcian blue staining of iPSCs undergoing chondrogenic differentiation over 21 days. B, Gene expression for pluripotency genes Nanog and Sox2 , mesenchymal marker Vim , and chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Mean ± SEM, n = 5 per group, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Journal: Stem cells (Dayton, Ohio)

    Article Title: Transient receptor potential vanilloid 4 as a regulator of induced pluripotent stem cell chondrogenesis

    doi: 10.1002/stem.3440

    Figure Lengend Snippet: Trpv4 expression during chondrogenesis of induced pluripotent stem cells (iPSCs). A, Alcian blue staining of iPSCs undergoing chondrogenic differentiation over 21 days. B, Gene expression for pluripotency genes Nanog and Sox2 , mesenchymal marker Vim , and chondrogenic markers Sox9, Acan , and Col2a1 , and Trpv4 . Mean ± SEM, n = 5 per group, groups not sharing the same letter are statistically different from one another (analysis of variance with Tukey's post hoc, P

    Article Snippet: After sorting, cells were lysed for RNA isolation and subsequent qRT-PCR to measure expression of Nanog, Sox9, Acan, Col2a1 , and Trpv4 as described above, or seeded on gelatin-coated coverslips for 48 hours for TRPV4 immunocytochemistry.

    Techniques: Expressing, Staining, Marker

    p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: p38 activation and macrophage phagocytosis in response to LPS is dependent on matrix stiffness. Phosphorylated and total A. p38 and B. JNK on various matrix stiffnesses in the physiologic range (1kPa, 8kPa, and 25kPa) from WT vs TRPV4 KO BMDMs quantified for LPS 15 minutes ( *p = 0.031). C. Macrophage phagocytosis of E. coli particles ± p38 inhibition (SB, BIRB) on various matrix stiffnesses ( *p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Activation Assay, Inhibition

    TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: TRPV4-mediated p38 MAPK and JNK molecular switch is regulated by dual-specificity phosphatase 1 (DUSP1). WT and TRPV4 KO BMDMs were incubated ± LPS as above for indicated time, and cells were lysed and analyzed by A. immunoblot for DUSP1 and B. band density quantified as DUSP1/GAPDH from immunoblot (n = 4) ( *p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Incubation

    TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: TRPV4 function protects against lung injury in a murine Pseudomonas aeruginosa pneumonia model. Sterile beads or P. aeruginosa (PA, PAM57–15) were instilled intratracheally in TRPV4 KO and age-matched female congenic WT mice with BAL and tissue harvest performed at Day 3 (injury phase). TRPV4 deleted mice (TRPV4 KO) have greater A. inflammatory cell infiltration and B. BAL total protein compared to WT (* p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Mouse Assay

    p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: p38 MAPK and JNK are differentially regulated by TRPV4 after LPS or Pseudomonas aeruginosa . BMDMs were incubated ± LPS as above for indicated time cultured on tissue culture-treated plastic, and cells were lysed and analyzed by immunoblot for A. phosphorylated and total p38, ERK, and JNK compared to WT BMDMs (whole cell lysate). Band density quantified from immunoblot (n = 3–6) for B. p-p38/total p38 ( *p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Incubation, Cell Culture

    TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: TRPV4 mediates phagocytosis after LPS in healthy human through p38 MAPK. Monocyte derived and alveolar macrophages from healthy (n = 6) control subjects were incubated ± LPS ± TRPV4 inhibitor, HC, and phagocytosis of E. coli particles was measured in A. monocyte-derived and B. alveolar macrophages in healthy controls. HC alone had no effect. Representative immunoblot for phosphorylated and total p38 in C. healthy monocyte derived macrophages ± LPS 15 minutes and D. band density quantified ( *p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Derivative Assay, Incubation

    TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: TRPV4 mediates clearance of P. aeruginosa by macrophages. WT and TRPV4 KO mice were intratracheally administered ±GFP P. aeruginosa for 3 days. Representative confocal images of whole lung lavage cytospins of macrophages (open arrowhead) and neutrophils (filled arrowhead) in WT mice given IT sterile beads or GFP- P. aeruginosa after immunofluorescence with A. TRPV4 extracellular antibody (green, TRPV4) and C. anti-GFP (green, GFP P. aeruginosa ; anti-CD45, red; dapi, blue). B, D. Quantification of A, C . * , # p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Mouse Assay, Immunofluorescence

    TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: TRPV4 Protects the Lung from Bacterial Pneumonia via MAPK Molecular Pathway Switching

    doi: 10.4049/jimmunol.1901033

    Figure Lengend Snippet: TRPV4 modulates pro-inflammatory cytokine production through JNK. BMDMs were incubated ± LPS (100ng/mL, 24h) ± JNK inhibitor, SP600125 (20μM, 25h) ± p38 inhibitor, SB203580 (10μM, 25h), cultured on cell culture-treated plastic, and cytokines measured via ELISA. IL-6, CXCL2, and CXCL1 secretion ± LPS in A. WT and TRPV4 KO BMDMs and B. WT BMDMs ± SP600125 ± SB203580 ( *, # p

    Article Snippet: The following primary antibodies were purchased: intracellular TRPV4 (Alomone Labs, Jerusalem, Israel), extracellular TRPV4 (Alomone Labs, Jerusalem, Israel), anti-phospho p38 (Thr180/Tyr182, Cell Signaling, MA), anti-p38 (Santa Cruz, CA), anti-phospho JNK (Cell Signaling), anti-JNK (Cell Signaling), anti-phospho ERK (Santa Cruz), anti-ERK (Cell Signaling), anti-phospho MK2 (Cell Signaling), anti-MK2 (Cell Signaling), anti-phospho MKK3/MKK6 (Cell Signaling), anti-MKK3 (Cell Signaling), anti-MKK6 (Cell Signaling), anti-GAPDH (Fitzgerald Industries International, Acton, MA), anti-DUSP1/MKP1 (Santa Cruz, CA), α-CD45 (BD Biosciences), and purified rabbit IgG from mouse serum (Sigma-Aldrich, St. Louis, MO).

    Techniques: Incubation, Cell Culture, Enzyme-linked Immunosorbent Assay

    Transwell assays demonstrated that TRPV4 down-regulation greatly inhibited invasion abilities of gastric cancer cells. ( A and B ) Representative images of invasive cells following transfection with shTRPV4 or shCtrl. Magnification, ×200. ( C and D ) The column diagram of the numbers of invasive cells following transfection with shTRPV4 or shCtrl. **P

    Journal: OncoTargets and therapy

    Article Title: TRPV4 Overexpression Promotes Metastasis Through Epithelial–Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis

    doi: 10.2147/OTT.S256918

    Figure Lengend Snippet: Transwell assays demonstrated that TRPV4 down-regulation greatly inhibited invasion abilities of gastric cancer cells. ( A and B ) Representative images of invasive cells following transfection with shTRPV4 or shCtrl. Magnification, ×200. ( C and D ) The column diagram of the numbers of invasive cells following transfection with shTRPV4 or shCtrl. **P

    Article Snippet: After blocking with 20% bovine serum albumin (BSA), these pretreated slides were incubated at 4°C overnight with antibodies against TRPV4 (1:100 dilution, #ACC-034-AO, Alomone labs), E-cadherin (1:50 dilution, clone NCH-38, Dako), and vimentin (1:100 dilution, clone V9, Dako), followed by incubation with the HRP-conjugated secondary antibody (Dako).

    Techniques: Transfection

    Detection of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues by IHC staining of tissue microarrays. ( A ) Representative images of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues. (a, b) Weakly focal positive TRPV4 expression in adjacent noncancerous gastric epithelia. (c, d) Strongly positive TRPV4 expression in a case of gastric adenocarcinoma. ( B ) Scatterplots of IHC scores of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues. ( C ) Percents of tissue samples with high TRPV4 expression and low TRPV4 expression based on the cut-off value of IHC scores in gastric adenocarcinoma tissues and adjacent noncancerous tissues (***P

    Journal: OncoTargets and therapy

    Article Title: TRPV4 Overexpression Promotes Metastasis Through Epithelial–Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis

    doi: 10.2147/OTT.S256918

    Figure Lengend Snippet: Detection of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues by IHC staining of tissue microarrays. ( A ) Representative images of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues. (a, b) Weakly focal positive TRPV4 expression in adjacent noncancerous gastric epithelia. (c, d) Strongly positive TRPV4 expression in a case of gastric adenocarcinoma. ( B ) Scatterplots of IHC scores of TRPV4 expression in gastric adenocarcinoma tissues and adjacent noncancerous tissues. ( C ) Percents of tissue samples with high TRPV4 expression and low TRPV4 expression based on the cut-off value of IHC scores in gastric adenocarcinoma tissues and adjacent noncancerous tissues (***P

    Article Snippet: After blocking with 20% bovine serum albumin (BSA), these pretreated slides were incubated at 4°C overnight with antibodies against TRPV4 (1:100 dilution, #ACC-034-AO, Alomone labs), E-cadherin (1:50 dilution, clone NCH-38, Dako), and vimentin (1:100 dilution, clone V9, Dako), followed by incubation with the HRP-conjugated secondary antibody (Dako).

    Techniques: Expressing, Immunohistochemistry, Staining

    The protein expression of TRPV4 in gastric cell lines and down-regulation of TPRV4 inhibited proliferation of gastric cancer cells. ( A ) The protein expression levels of TPRV4 were detected in gastric cancer cell lines (HGC-27 and MGC-803) and normal gastric mucosa cell GES-1 by Western blot. **P

    Journal: OncoTargets and therapy

    Article Title: TRPV4 Overexpression Promotes Metastasis Through Epithelial–Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis

    doi: 10.2147/OTT.S256918

    Figure Lengend Snippet: The protein expression of TRPV4 in gastric cell lines and down-regulation of TPRV4 inhibited proliferation of gastric cancer cells. ( A ) The protein expression levels of TPRV4 were detected in gastric cancer cell lines (HGC-27 and MGC-803) and normal gastric mucosa cell GES-1 by Western blot. **P

    Article Snippet: After blocking with 20% bovine serum albumin (BSA), these pretreated slides were incubated at 4°C overnight with antibodies against TRPV4 (1:100 dilution, #ACC-034-AO, Alomone labs), E-cadherin (1:50 dilution, clone NCH-38, Dako), and vimentin (1:100 dilution, clone V9, Dako), followed by incubation with the HRP-conjugated secondary antibody (Dako).

    Techniques: Expressing, Western Blot

    Survival curves using the Kaplan–Meier method by Log rank test. ( A and B ) The patients with high TRPV4 expression had shorter overall survival and disease-free survival than those with low TRPV4 expression. ( C and D ) The patients with low E-cadherin expression had shorter overall survival and disease-free survival than those with high E-cadherin expression. ( E and F ) The patients with high vimentin expression had shorter overall survival and disease-free survival than those with low vimentin expression. ( G ) Overall survival analysis of TRPV4 gene in gastric cancer obtained from Kaplan–Meier Plotter online ( http://kmplot.com/analysis/ ). *P

    Journal: OncoTargets and therapy

    Article Title: TRPV4 Overexpression Promotes Metastasis Through Epithelial–Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis

    doi: 10.2147/OTT.S256918

    Figure Lengend Snippet: Survival curves using the Kaplan–Meier method by Log rank test. ( A and B ) The patients with high TRPV4 expression had shorter overall survival and disease-free survival than those with low TRPV4 expression. ( C and D ) The patients with low E-cadherin expression had shorter overall survival and disease-free survival than those with high E-cadherin expression. ( E and F ) The patients with high vimentin expression had shorter overall survival and disease-free survival than those with low vimentin expression. ( G ) Overall survival analysis of TRPV4 gene in gastric cancer obtained from Kaplan–Meier Plotter online ( http://kmplot.com/analysis/ ). *P

    Article Snippet: After blocking with 20% bovine serum albumin (BSA), these pretreated slides were incubated at 4°C overnight with antibodies against TRPV4 (1:100 dilution, #ACC-034-AO, Alomone labs), E-cadherin (1:50 dilution, clone NCH-38, Dako), and vimentin (1:100 dilution, clone V9, Dako), followed by incubation with the HRP-conjugated secondary antibody (Dako).

    Techniques: Expressing

    Representation images of TRPV4, E-cadherin and vimentin expression in gastric cancer tissues by immunohistochemical staining. Magnification, ×400. ( A – C ) High TRPV4 expression in a case of poor differentiated gastric adenocarcinoma with loss expression of E-cadherin and positive vimentin expression. ( D – F ) Low TRPV4 expression in a case of signet ring cell carcinoma with high E-cadherin expression and negative Vimentin expression. Abbreviation: TRPV4, transient receptor potential vanilloid 4.

    Journal: OncoTargets and therapy

    Article Title: TRPV4 Overexpression Promotes Metastasis Through Epithelial–Mesenchymal Transition in Gastric Cancer and Correlates with Poor Prognosis

    doi: 10.2147/OTT.S256918

    Figure Lengend Snippet: Representation images of TRPV4, E-cadherin and vimentin expression in gastric cancer tissues by immunohistochemical staining. Magnification, ×400. ( A – C ) High TRPV4 expression in a case of poor differentiated gastric adenocarcinoma with loss expression of E-cadherin and positive vimentin expression. ( D – F ) Low TRPV4 expression in a case of signet ring cell carcinoma with high E-cadherin expression and negative Vimentin expression. Abbreviation: TRPV4, transient receptor potential vanilloid 4.

    Article Snippet: After blocking with 20% bovine serum albumin (BSA), these pretreated slides were incubated at 4°C overnight with antibodies against TRPV4 (1:100 dilution, #ACC-034-AO, Alomone labs), E-cadherin (1:50 dilution, clone NCH-38, Dako), and vimentin (1:100 dilution, clone V9, Dako), followed by incubation with the HRP-conjugated secondary antibody (Dako).

    Techniques: Expressing, Immunohistochemistry, Staining