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. 2021 Dec 3;9:767006. doi: 10.3389/fcell.2021.767006

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Copyright © 2021 Wang, Li, Li, Li, Gao, Bao, Wang, Liu, Xue and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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CCG targeted TAZ to facilitate osteogenic differentiation of BMSCs in vitro. (A) MTT assays presented cell viabilities after CCG administration during osteogenesis of BMSCs. (B, C) Representative images of AR-S results in different mice groups. Scale bar: 100 μm. (D, E) Relative mRNA levels of TAZ, RUNX2, and OCN with or without CCG treatment. (F–I) TAZ, RUNX2, and OCN expression in protein levels with or without CCG treatment. *p < 0.05 vs. the control group. (J–L) SiTAZ plasmid significantly knocked down the mRNA and protein levels of TAZ during the osteogenesis of BMSCs. (M–Q) SiTAZ discounted the CCG induced up-regulation of RUNX2 and OCN. (R, S) Representative images of AR-S showed the differences of calcium deposits in different groups. Bar graphs showed the means ± SD from three independent experiments. Scale bar: 100 μm (n = 3) *p < 0.05 vs. the Vehicle group; #p < 0.05 vs. the Vehicle + CCG group.