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. Author manuscript; available in PMC: 2018 Jan 2.
Published in final edited form as: Bone. 2015 Nov 10;83:162–170. doi: 10.1016/j.bone.2015.11.007

Fig. 3.

Fig. 3

The effect of CCN4 on TGF-β3-SMAD signaling pathway in vitro. hBMSCs were transduced with adCCN4 (A) or siCCN4 (B) for 2 days. (A, B) Transduced-hBMSCs in monolayer culture were treated with 10 ng/mL of TGF-β3 for 10 min, and cellular proteins were collected for detection of SMAD2/3 activity. β-ACTIN was used as protein loading control. (C) Chondrocytes were collected from mandibular condylar cartilage of newborn WT and Ccn4-KO mice, and stimulated with TGF-β3 for 10 min. The cellular proteins were collected for analysis of TGF-β3-induced phosphorylation of SMAD2/3. SMAD2/3 activity was decreased in chondrocytes derived from Ccn4-KO mice, compared to WT mice.