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Fig. 3 | Cell Communication and Signaling

Fig. 3

From: Unveiling the transcriptomic landscape and the potential antagonist feedback mechanisms of TGF-β superfamily signaling module in bone and osteoporosis

Fig. 3

BMP8 activates both SMAD pathways in bone marrow-derived mesenchymal stem cells. A–C Detection and autocrine function of BMP8 proteins in bone cells. A Conditioned media collected from bone marrow (BM) cells or C3H10T1/2 cells without or with Bmp8a knockdown were subjected to immunoblotting using the antibody against BMP8. B Knockdown efficiency of Bmp8a in C3H10T1/2. ***P < 0.001. C Knockdown of Bmp8a dampens the phosphorylation levels of both SMAD1/5/8 and SMAD2/3 endogenously. To confirm that the BMP8-induced SMAD signaling occurs in MSCs, primary human BM-MSCs (D), primary mouse BM-MSCs (E) or C3H10T1/2 cells (F) were treated with graded doses of BMP8A, BMP2, activin A or TGF-β1 as indicated. The cell lysates were then subjected to immunoblotting using antibody against phosphorylated SMAD1/5/8 (upper panel) or phosphorylated SMAD2/3 (lower panel). Total forms of SMADs and β-actin served as loading controls

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Cell Communication and Signaling

ISSN: 1478-811X