pdgfa Search Results


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Gold Biotechnology Inc pdgfa
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Novus Biologicals recombinant mouse pdgfa
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Proteintech human growth factors
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Novus Biologicals pdgf a
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Thermo Fisher gene exp pdgfa mm00435540 m1
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Thermo Fisher gene exp pdgfa mm01205760 m1
Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A <t>(PDGFA)</t> , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005
Gene Exp Pdgfa Mm01205760 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher gene exp pdgfa hs00964426 m1
Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A <t>(PDGFA)</t> , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005
Gene Exp Pdgfa Hs00964426 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher gene exp pdgfa hs00234994 m1
Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A <t>(PDGFA)</t> , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005
Gene Exp Pdgfa Hs00234994 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher gene exp pdgfa hs00236997 m1
Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A <t>(PDGFA)</t> , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005
Gene Exp Pdgfa Hs00236997 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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OriGene pdgfa
Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A <t>(PDGFA)</t> , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005
Pdgfa, supplied by OriGene, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A (PDGFA) , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005

Journal: Cell Death & Disease

Article Title: Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy

doi: 10.1038/s41419-018-0792-6

Figure Lengend Snippet: Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A (PDGFA) , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005

Article Snippet: All mRNA-specific FAM-labeled primers/probe were purchased from Applied Biosystems and detected cDNA from the following genes: Ctgf (Mm01192933_g1), Pdgfa (Mm01205760_m1), Pdgfb (Mm00440677_m1), Tgfb1 (Mm01178820_m1), Col1a1 (Mm00801666_g1), Col3a1 (Mm01254476_m1), Fn1 (Mm01256744_m1), Adgre1 (Mm00802529_m1), PDGFA (Hs00964426_m1), CTGF (Hs01026927_g1), PDGFB (Hs00966522_m1), TGFB1 (Hs00998133_m1), COL1A1 (Hs00164004_m1), COL3A1 (Hs00943809_m1), FN1 (Hs01549976_m1), ACTA (Hs00426835_g1), MMP9 (Hs00957562_m1), MMP2 (Hs01548727_m1), MMP1 (Hs00899658_m1), TIMP-1 (Hs99999139_m1), TIMP-2 (Hs00234278_m1), ADAM-12 (Hs01106101_m1), ADAM-17 (Hs01041915_m1), TP53 (Hs01034249_m1).

Techniques: Cell Culture, Derivative Assay, Migration, Wound Healing Assay, Expressing, Produced, Control

Collagen type I alpha 1 chain (Col1a1), Collagen type III alpha 1 chain ( Col3a1 ), Fibronectin 1 ( Fn1 ), Platelet-derived growth factor A ( Pdgfa ), Platelet-derived growth factor B ( Pdgfb ), Connective tissue growth factor ( Ctgf ), Transforming growth factor beta 1 ( Tgfβ1 ), and Adhesion G protein-coupled receptor E1 ( Adgre1 ) showed changes in relative abundance following nintedanib in quadriceps ( a–h ), diaphragm ( i–p ), and tibialis anterior ( q–y ). Col1a1, Col3a1, Pdgfa, Tgfb1, and Adgre1 gene expression was increased in mdx mice compared with WT . Col1a1, Col3a1, Pdgfa, Pdgfb, Tgfb1, and Adgre1 expression was reduced in all muscles analyzed from nintedanib-treated mdx mice compared with mdx mice. In contrast, Ctgf expression was increased in muscles from nintedanib-treated mdx mice compared with mdx mice. Data are expressed as means ± SD. Genetic background mouse strain C57BL (WT); n = 5, mdx mice (mdx), n = 5; nintedanib-treated mdx mice (mdx + Ninte), n = 7. * P < 0.05, ** P < 0.01, *** P < 0.005

Journal: Cell Death & Disease

Article Title: Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy

doi: 10.1038/s41419-018-0792-6

Figure Lengend Snippet: Collagen type I alpha 1 chain (Col1a1), Collagen type III alpha 1 chain ( Col3a1 ), Fibronectin 1 ( Fn1 ), Platelet-derived growth factor A ( Pdgfa ), Platelet-derived growth factor B ( Pdgfb ), Connective tissue growth factor ( Ctgf ), Transforming growth factor beta 1 ( Tgfβ1 ), and Adhesion G protein-coupled receptor E1 ( Adgre1 ) showed changes in relative abundance following nintedanib in quadriceps ( a–h ), diaphragm ( i–p ), and tibialis anterior ( q–y ). Col1a1, Col3a1, Pdgfa, Tgfb1, and Adgre1 gene expression was increased in mdx mice compared with WT . Col1a1, Col3a1, Pdgfa, Pdgfb, Tgfb1, and Adgre1 expression was reduced in all muscles analyzed from nintedanib-treated mdx mice compared with mdx mice. In contrast, Ctgf expression was increased in muscles from nintedanib-treated mdx mice compared with mdx mice. Data are expressed as means ± SD. Genetic background mouse strain C57BL (WT); n = 5, mdx mice (mdx), n = 5; nintedanib-treated mdx mice (mdx + Ninte), n = 7. * P < 0.05, ** P < 0.01, *** P < 0.005

Article Snippet: All mRNA-specific FAM-labeled primers/probe were purchased from Applied Biosystems and detected cDNA from the following genes: Ctgf (Mm01192933_g1), Pdgfa (Mm01205760_m1), Pdgfb (Mm00440677_m1), Tgfb1 (Mm01178820_m1), Col1a1 (Mm00801666_g1), Col3a1 (Mm01254476_m1), Fn1 (Mm01256744_m1), Adgre1 (Mm00802529_m1), PDGFA (Hs00964426_m1), CTGF (Hs01026927_g1), PDGFB (Hs00966522_m1), TGFB1 (Hs00998133_m1), COL1A1 (Hs00164004_m1), COL3A1 (Hs00943809_m1), FN1 (Hs01549976_m1), ACTA (Hs00426835_g1), MMP9 (Hs00957562_m1), MMP2 (Hs01548727_m1), MMP1 (Hs00899658_m1), TIMP-1 (Hs99999139_m1), TIMP-2 (Hs00234278_m1), ADAM-12 (Hs01106101_m1), ADAM-17 (Hs01041915_m1), TP53 (Hs01034249_m1).

Techniques: Derivative Assay, Gene Expression, Expressing, Muscles

Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A (PDGFA) , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005

Journal: Cell Death & Disease

Article Title: Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy

doi: 10.1038/s41419-018-0792-6

Figure Lengend Snippet: Fibroblasts proliferation was analyzed after 2, 4, and 6 days of culture ( a–d ). We cultured fibroblast with increasing concentrations of nintedanib in a culture containing 10% fetal bovine serum (FBS) and we observed decreased fibroblast proliferation after 4 and 6 days in a dose-dependent manner ( a ). Fibroblasts were cultured in the presence of platelet-derived growth factor AA (PDGF-AA, 10 ng/mL) ( b ), basic fibroblast growth factor (FGFb, 10 ng/mL),( c) or vascular endothelial growth factor A (VEGF-A, 50 ng/mL) ( d ) with 1% FBS with or without nintedanib 0.4 μM. Only PDGF-AA increased cell proliferation, an effect that was reversed with the addition of nintedanib to the culture. Fibroblast migration was analyzed using a scratch assay. Nintedanid treatment at 0.4 μM reverted the promigratory effect of PDGF-AA, FGFb, VEGF, and CTGF ( e ). Representative images of this assay are shown in ( f ). Nintedanib treatment at 0.4 μM (blue bars) reverted the effect of PDGF-AA in the expression of ADAM metallopeptidase domain 17 ( ADAM-17) , tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) ( g ). Nintedanib treatment at 0.4 μM (blue bars) produced a statistically significant reduction of collagen type I alpha 1 chain (COL1A1) , collagen type III alpha 1 chain (COL3A1) , fibronectin 1 ( FN1) , platelet-derived growth factor A (PDGFA) , connective tissue growth factor (CTGF) , transforming growth factor beta 1 (TGFβ1) expression compared with control samples (black bars) analyzed by qPCR ( h ). Data are expressed as means ± SD. N = 3 per group. * P < 0.05, ** P < 0.01, *** P < 0.005

Article Snippet: All mRNA-specific FAM-labeled primers/probe were purchased from Applied Biosystems and detected cDNA from the following genes: Ctgf (Mm01192933_g1), Pdgfa (Mm01205760_m1), Pdgfb (Mm00440677_m1), Tgfb1 (Mm01178820_m1), Col1a1 (Mm00801666_g1), Col3a1 (Mm01254476_m1), Fn1 (Mm01256744_m1), Adgre1 (Mm00802529_m1), PDGFA (Hs00964426_m1), CTGF (Hs01026927_g1), PDGFB (Hs00966522_m1), TGFB1 (Hs00998133_m1), COL1A1 (Hs00164004_m1), COL3A1 (Hs00943809_m1), FN1 (Hs01549976_m1), ACTA (Hs00426835_g1), MMP9 (Hs00957562_m1), MMP2 (Hs01548727_m1), MMP1 (Hs00899658_m1), TIMP-1 (Hs99999139_m1), TIMP-2 (Hs00234278_m1), ADAM-12 (Hs01106101_m1), ADAM-17 (Hs01041915_m1), TP53 (Hs01034249_m1).

Techniques: Cell Culture, Derivative Assay, Migration, Wound Healing Assay, Expressing, Produced, Control

Collagen type I alpha 1 chain (Col1a1), Collagen type III alpha 1 chain ( Col3a1 ), Fibronectin 1 ( Fn1 ), Platelet-derived growth factor A ( Pdgfa ), Platelet-derived growth factor B ( Pdgfb ), Connective tissue growth factor ( Ctgf ), Transforming growth factor beta 1 ( Tgfβ1 ), and Adhesion G protein-coupled receptor E1 ( Adgre1 ) showed changes in relative abundance following nintedanib in quadriceps ( a–h ), diaphragm ( i–p ), and tibialis anterior ( q–y ). Col1a1, Col3a1, Pdgfa, Tgfb1, and Adgre1 gene expression was increased in mdx mice compared with WT . Col1a1, Col3a1, Pdgfa, Pdgfb, Tgfb1, and Adgre1 expression was reduced in all muscles analyzed from nintedanib-treated mdx mice compared with mdx mice. In contrast, Ctgf expression was increased in muscles from nintedanib-treated mdx mice compared with mdx mice. Data are expressed as means ± SD. Genetic background mouse strain C57BL (WT); n = 5, mdx mice (mdx), n = 5; nintedanib-treated mdx mice (mdx + Ninte), n = 7. * P < 0.05, ** P < 0.01, *** P < 0.005

Journal: Cell Death & Disease

Article Title: Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy

doi: 10.1038/s41419-018-0792-6

Figure Lengend Snippet: Collagen type I alpha 1 chain (Col1a1), Collagen type III alpha 1 chain ( Col3a1 ), Fibronectin 1 ( Fn1 ), Platelet-derived growth factor A ( Pdgfa ), Platelet-derived growth factor B ( Pdgfb ), Connective tissue growth factor ( Ctgf ), Transforming growth factor beta 1 ( Tgfβ1 ), and Adhesion G protein-coupled receptor E1 ( Adgre1 ) showed changes in relative abundance following nintedanib in quadriceps ( a–h ), diaphragm ( i–p ), and tibialis anterior ( q–y ). Col1a1, Col3a1, Pdgfa, Tgfb1, and Adgre1 gene expression was increased in mdx mice compared with WT . Col1a1, Col3a1, Pdgfa, Pdgfb, Tgfb1, and Adgre1 expression was reduced in all muscles analyzed from nintedanib-treated mdx mice compared with mdx mice. In contrast, Ctgf expression was increased in muscles from nintedanib-treated mdx mice compared with mdx mice. Data are expressed as means ± SD. Genetic background mouse strain C57BL (WT); n = 5, mdx mice (mdx), n = 5; nintedanib-treated mdx mice (mdx + Ninte), n = 7. * P < 0.05, ** P < 0.01, *** P < 0.005

Article Snippet: All mRNA-specific FAM-labeled primers/probe were purchased from Applied Biosystems and detected cDNA from the following genes: Ctgf (Mm01192933_g1), Pdgfa (Mm01205760_m1), Pdgfb (Mm00440677_m1), Tgfb1 (Mm01178820_m1), Col1a1 (Mm00801666_g1), Col3a1 (Mm01254476_m1), Fn1 (Mm01256744_m1), Adgre1 (Mm00802529_m1), PDGFA (Hs00964426_m1), CTGF (Hs01026927_g1), PDGFB (Hs00966522_m1), TGFB1 (Hs00998133_m1), COL1A1 (Hs00164004_m1), COL3A1 (Hs00943809_m1), FN1 (Hs01549976_m1), ACTA (Hs00426835_g1), MMP9 (Hs00957562_m1), MMP2 (Hs01548727_m1), MMP1 (Hs00899658_m1), TIMP-1 (Hs99999139_m1), TIMP-2 (Hs00234278_m1), ADAM-12 (Hs01106101_m1), ADAM-17 (Hs01041915_m1), TP53 (Hs01034249_m1).

Techniques: Derivative Assay, Gene Expression, Expressing, Muscles