摘要
Gap junction(GJ)has been indicated to have an intimate correlation with adhesion junction.However,the direct interaction between them partially remains elusive.In the current study,we aimed to elucidate the role of N-cadherin,one of the core components in adhesion junction,in mediating connexin 43,one of the functional constituents in gap junction,via transforming growth factor-β1(TGF-β1)induction in osteoblasts.We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43,and the enhancement of functional gap junctional intercellular communication(GJIC)triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line.Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell–cell contact.Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43.Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced.TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation,whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43.Overall,these data indicate the direct interactions between N-cadherin and Cx43,and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts.
基金
the funding of NSFC grants(81771047)to J.X.
