Inhibiting N-cadherin-mediated adhesion affects gap junction communication in isolated rat hearts

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• 作者：Hongjun Zhu (1)
  Hegui Wang (1)
  Xiwen Zhang (1)
  Xiaofeng Hou (1)
  Kejiang Cao (1)
  Jiangang Zou (1)
  
• 关键词：adherens junction ; connexin 43 ; gap junction ; N ; cadherin ; synthetic polypeptides
• 刊名：Molecules and Cells
• 出版年：2010
• 出版时间：September 2010
• 年：2010
• 卷：30
• 期：3
• 页码：193-200
• 全文大小：1959KB
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• 作者单位：Hongjun Zhu (1)
  Hegui Wang (1)
  Xiwen Zhang (1)
  Xiaofeng Hou (1)
  Kejiang Cao (1)
  Jiangang Zou (1)
  
  1. Department of Cardiology, First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, 210029, China
  
• ISSN：0219-1032

文摘

Cadherin-mediated adherens junctions is impaired concomitant with a decrease in connexin 43 (Cx43) in diseases or pathological processes. We have investigated the acute effects of adherens junction impairment in isolated rat hearts by introducing Ala-His-Ala-Val-Asp-NH2 (AHAVD, a synthetic peptide) as a specific inhibitor of N-cadherin. Effect of AHAVD on N-cadherin mediated adhension was analyzed by Cardiomy-ocyte aggregation assay. Laser confocal microscopy showed disrupted cell-cell contacts in cultured neonatal cardiomyocytes co-incubated with 0.2 mM AHAVD. In isolated adult rat hearts, Cx43 was redistributed along the bilateral of cardiomyocytes from the intercalated discs and significant dephosphorylation of Cx43 on serine368 occurred concomitantly with decreased gap junction (GJ) function in dose dependent manner after 1 h perfusion with AHAVD. These results indicate that impairing cad-herin-mediated adhesion by AHAVD rapidly results in Cx43 redistribution and dephosphorylation of serine368, thereby impairing GJ communication function.