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Novus Biologicals rabbit anti vitronectin nbp2 20866
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Promega rabbit anti-active tgf-β1
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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OriGene rabbit anti human collagen i r1038x
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Biorbyt rabbit antiserpinf2 orb101685
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Jackson Immuno hrp conjugated goat anti rabbit igg
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Jackson Immuno hrp conjugated goat antimouse igg
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Cell Signaling Technology Inc rabbit anti p smad3 ps465 467 138d4
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Jackson Immuno hrp conjugated goat anti mouse igg
A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active <t>Tgf-β1</t> (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).
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Image Search Results


A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active Tgf-β1 (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).

Journal: EMBO Molecular Medicine

Article Title: Losartan ameliorates dystrophic epidermolysis bullosa and uncovers new disease mechanisms

doi: 10.15252/emmm.201505061

Figure Lengend Snippet: A–D C7-hypomorphic mice were treated with losartan for 7 weeks, and the forepaws of age-matched untreated, losartan-treated, and wild-type mice were subjected to immunofluorescence staining with antibodies to active thrombospondin 1 (Tsp1, green) (A), active Tgf-β1 (green) (B), TGF-β receptor II (Tgfbr2, red) (C), and phospho-Smad2 and 3 (P-Smad2/3, red) (D). The nuclei were counterstained with DAPI (blue). Images were acquired with a 20× objective (scale bar = 100 μm) (A), with a 4× objective (scale bar = 200 μm) (B, D), and with a 40× objective (scale bar = 50 μm) (C). The bar graphs on the right show quantification of the stainings in the left panel of (B) and (D). Paired values were normalized to the staining intensity of untreated C7-hypomorphic paws, which were set to 100%. Values represent mean ± S.E.M., n = 6, paired Student’s t -test, *** P -value wild-type vs. C7-hypomorph receiving no treatment = 0.0004; *** P -value losartan treatment vs. no treatment = 0.0005 (B). Values represent mean ± S.E.M., n ≥ 7, unpaired t -test with Welch’s correction used, *** P -value wild-type vs. C7-hypomorph < 0.0001; *** P -value C7-hypomorph + losartan vs. C7-hypomorph = 0.0002; ** P -value wild-type vs. C7-hypomorph + losartan = 0.0016 (D).

Article Snippet: The following antibodies were used: mouse anti-human TSP1 clone A6.1, rabbit anti-P-SMAD2/3 (sc-11769R), rabbit anti-SMAD2/3 (FL-425), and goat anti-LRG1 (P-16) (Santa Cruz Biotechnology, Santa Cruz, CA, USA); rabbit anti-human collagen I (R1038X) (Acris Antibodies, Herford, Germany); rabbit anti-active TGF-β1 (Promega, Madison, WI, USA); mouse anti-human β-actin clone AC-15, mouse anti-human total ERK1/2 clone ERK-NP2, mouse anti-human P-ERK1/2 clone ERK-PT 115, rat anti-mouse tenascin-C clone 578, and mouse anti-human serpin F2 (mAb1470; R&D systems, Minneapolis, MN, USA); rabbit anti-human IL-6 (ab6672), rabbit anti-human fibronectin (ab2413), rabbit anti-human TGFBR2 (ab28382), and rabbit anti-β-tubulin (ab6046) (Abcam, Cambridge, UK); rabbit anti-P-SMAD3 (pS465/467) (138D4) (Cell Signaling, Danvers, MA, USA); rabbit anti-P-SMAD2 (pS423/425) (EP823Y) (Epitomics, Burlingame, CA, USA); rat anti-mouse Cd11b clone M1/70 (BD Biosciences, Heidelberg, Germany); rat anti-mouse C1q clone 7H8 (Hycult Biotech, Uden, the Netherlands); rabbit anti-collagen VII (234192) (Merck Millipore, Billerica, MA, USA); rabbit anti-vitronectin (NBP2-20866) (Novus Biologicals, Littelton, CO, USA); rabbit anti-SERPINF2 (orb101685) (Biorbyt, Cambridge, UK); Cy3-conjugated mouse anti-αSMA clone 2B1 (Sigma-Aldrich, St. Louis, MO, USA); HRP-conjugated goat anti-rabbit IgG and HRP-conjugated goat anti-mouse IgG (Jackson ImmunoResearch, West Grove, PA, USA); and Alexa 488- or 546-conjugated goat anti-rat, anti-rabbit, or anti-mouse IgG (Molecular Probes, Eugene, OR, USA).

Techniques: Immunofluorescence, Staining