XXXX Up-Regulation Induced by a High Concentration of @entity619 Promotes @entity35 Tendon Stem Cells to Differentiate Into Adipocytes.

@entity13557 @entity20134 @entity9096 @entity9170 @entity16596 @entity619 @entity397 @entity35 @entity60974 @entity29972 @entity12891
BACKGROUND/AIMS: @entity619 ( @entity9170 )-induced spontaneous @entity397 and decreased self-repair capability is very common in clinical practice. The metaplasia of adipose tissue in the ruptured tendon indicates that @entity9170 may induce tendon stem cells (TSCs) to differentiate into adipocytes, but the mechanism remains unclear. In the present study, we used in vitro methods to investigate the effects of @entity9170 on @entity35 TSC differentiation and the molecular mechanisms underlying this process. METHODS: First, we used qPCR and Western blotting to detect the expression of the adipogenic differentiation markers @entity12891 and @entity16596 after treating the TSCs with @entity9170 . Oil red staining was used to confirm that high concentration @entity9170 promoted adipogenic differentiation of @entity35 TSCs. Next, we used qPCR and Western blotting to detect the effect of a high concentration of @entity619 on molecules related to the canonical @entity29972 -catenin pathway in TSCs. RESULTS: Treating @entity35 TSCs with @entity9170 promoted the synthesis of the inhibitory molecule @entity60974 ( @entity60974 ) at the mRNA and protein levels. Western blotting results further showed that @entity9170 downregulated the cellular signaling molecule phosphorylated glycogen synthase kinase-3b (P-GSK-3 b (ser9)), upregulated P- @entity9096 (tyr216), and downregulated the pivotal signaling molecule b-catenin. Furthermore, @entity60974 knockdown attenuated @entity9170 -induced inhibition of the canonical @entity29972 -catenin pathway and of the adipogenic differentiation of TSCs. @entity13557 ( @entity20134 , a @entity9096 inhibitor) reduced @entity9170 -induced inhibition of the classical @entity29972 -catenin pathway in TSCs and of the differentiation of TSCs to adipocytes. CONCLUSION: In conclusion, by upregulating @entity60974 expression, reducing the level of P- @entity9096 (ser9), and increasing the level of P- @entity9096 (tyr216), @entity9170 causes the degradation of b-catenin, the central molecule of the classical @entity29972 pathway, thereby inducing @entity35 TSCs to differentiate into adipocytes.
