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Transforming growth factor-β1-induced N-cadherin drives cell–cell communication through connexin43 in osteoblast lineage
International Journal of Oral Science ( IF 14.9 ) Pub Date : 2021-04-13 , DOI: 10.1038/s41368-021-00119-3
Yueyi Yang , Wenjing Liu , JieYa Wei , Yujia Cui , Demao Zhang , Jing Xie

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.



中文翻译:

转化生长因子-β1诱导的N-钙黏着蛋白通过成骨细胞谱系中的连接蛋白43驱动细胞间的通信

间隙连接(GJ)已被证明与粘附连接密切相关。但是,它们之间的直接交互仍然难以捉摸。在本研究中,我们旨在阐明N-钙粘着蛋白(粘附连接的核心成分之一)通过转化生长因子-β1(TGF-β1)介导间隙连接中的功能性成分之一连接蛋白43的作用。诱导成骨细胞。我们首先阐明了TGF-β1诱导的N-钙黏着蛋白的表达,并证实了Cx43的上调,以及TGF-β1触发的原代成骨细胞和MC3T3细胞系中功能间隙连接细胞间通讯(GJIC)的增强。共定位分析和Co-IP实验表明,N-钙粘着蛋白在细胞间接触部位与Cx43相互作用。siRNA干扰敲低N-cadherin降低了Cx43的表达并取消了TGF-β1对Cx43的促进作用。活的原代成骨细胞和MC3T3细胞系中的功能性GJIC也减少了。TGF-β1诱导的N-钙黏着蛋白和Cx43的增加是通过Smad3激活,而通过使用siRNA抑制Smad3信号转导会降低N-钙黏着蛋白和Cx43的表达。总体而言,这些数据表明N-钙粘蛋白和Cx43之间存在直接的相互作用,并揭示了活骨细胞功能间隙连接中黏附连接的干预作用。而通过使用siRNA敲低Smad3信号传导可降低N-钙粘蛋白和Cx43的表达。总体而言,这些数据表明N-钙粘蛋白和Cx43之间存在直接的相互作用,并揭示了活骨细胞功能间隙连接中黏附连接的干预作用。而通过使用siRNA敲低Smad3信号传导可降低N-钙粘蛋白和Cx43的表达。总体而言,这些数据表明N-钙粘蛋白和Cx43之间存在直接的相互作用,并揭示了活骨细胞功能间隙连接中黏附连接的干预作用。

更新日期:2021-04-14
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