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. Author manuscript; available in PMC: 2019 Jul 31.
Published in final edited form as: Circulation. 2018 Jul 31;138(5):513–526. doi: 10.1161/CIRCULATIONAHA.117.031635

Figure 2. Bone Morphogenetic Protein 9 Attenuates TGFβ1 Induced Collagen Production in Human Cardiac Fibroblasts.

Figure 2

A) Representative immunoblots for bone morphogenetic protein 9 (BMP9), Endoglin, CD31, Periostin, Troponin T and GAPDH in human cardiomyocytes (CM), cardiac fibroblasts (CF), and endothelial cells (EC). B) Type I collagen mRNA expression in human cardiac fibroblasts stimulated with TGF-β1 at 10 ng/ml, recombinant human BMP9 (rhBMP9) at 1, 5, 10 ng/ml, or both C) Quantitation of type I collagen protein expression normalized to GAPDH expression with representative immunoblots. D) Type I collagen mRNA expression in human cardiac fibroblasts following knockdown of BMP9 expression with siBMP9 compared to scrambled siRNA (scr-siRNA). E) Quantitation and representative immunoblots of type I collagen protein expression normalized to GAPDH expression. Data for panels B–E represent an average of 3 independent experiments and are expressed as fold change vs. control. Panels B–C: p<0.05: *, vs. No TGF-β1; †, vs. TGF-β1. Panels D–E: p<0.05: *, vs. Control scr-siRNA; †, vs. Control siBMP9.