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Connexin 43 expressed in endothelial cells modulates monocyte-endothelial adhesion by regulating cell adhesion proteins

Connexin 43 expressed in endothelial cells modulates monocyte-endothelial adhesion by regulating cell adhesion proteins

Authors :
Gangjian Luo
Chenfang Luo
Mian Ge
Guoliang Sun
Dongdong Yuan
Rui Zhang
Ziqing Hei
Source :
Molecular Medicine Reports. 12:7146-7152
Publication Year :
2015
Publisher :
Spandidos Publications, 2015.

Abstract

Adhesion between circulating monocytes and vascular endothelial cells is a key initiator of atherosclerosis. In our previous studies, it was demonstrated that the expression of connexin (Cx)43 in monocytes modulates cell adhesion, however, the effects of the expression of Cx43 in endothelial cells remains to be elucidated. Therefore, the present study investigated the role of the expression of Cx43 in endothelial cells in the process of cell adhesion. A total of four different methods with distinct mechanisms were used to change the function and expression of Cx43 channels in human umbilical vein endothelial cells: Cx43 channel inhibitor (oleamide), enhancer (retinoic acid), overexpression of Cx43 by transfection with pcDNA‑Cx43 and knock‑down of the expression of Cx43 by small interfering RNA against Cx43. The results indicated that the upregulation of the expression of Cx43 enhanced monocyte‑endothelial adhesion and this was markedly decreased by downregulation of Cx43. This mechanism was associated with Cx43‑induced expression of vascular cell adhesion molecule‑1 and intercellular cell adhesion molecule‑1. The effects of Cx43 in endothelial cells was independent of Cx37 or Cx40. These experiments suggested that local regulation of endothelial Cx43 expression within the vasculature regulates monocyte‑endothelial adhesion, a critical event in the development of atherosclerosis and other inflammatory pathologies, with baseline adhesion set by the expression of Cx43. This balance may be crucial in controlling leukocyte involvement in inflammatory cascades.

Details

ISSN :
17913004 and 17912997
Volume :
12
Database :
OpenAIRE
Journal :
Molecular Medicine Reports
Accession number :
edsair.doi.dedup.....42fd0c7a04bc1b375cba38dea6d4ef1a
Full Text :
https://doi.org/10.3892/mmr.2015.4273