期刊
JOURNAL OF SURGICAL RESEARCH
卷 142, 期 1, 页码 137-142出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.jss.2006.11.007
关键词
atherosclerosis; connexins; coronary artery bypass graft; gap junctions; internal mammary artery; mitogen-activated protein kinase; saphenous vein; vascular smooth muscle cells
类别
资金
- NHLBI NIH HHS [R01HL073349, R01HL070885] Funding Source: Medline
Background. Changes in connexin expression have been found in vascular smooth muscle cells (VSMCs) during the progression of atherosclerotic lesion and intimal hyperplasia. It is our hypothesis that increased connexin43 expression following stimulation of VSMCs with Ang II and lGF-1 contributes to more proliferation in saphenous vein (SV) than in the internal mammary artery (IMA). Materials and method. Using immunohistochemistry, Western blot, and reverse-transcription polymerase chain reaction, we assessed the effect of Ang H and IGF-1 stimulation on connexin43 expression and the signaling pathways involved in VSMCs of SV and IMA. Results. Immunostaining demonstrated strong expression of connexin43 in SV compared with IMA after stimulation with Ang H and IGF-1. Ang 11 up-regulated the expression of connexin43 in VSMCs of SV in a dose-and time-dependent manner. This was inhibited by p38 and ERK MAP kinase inhibitors, SB203580 and PD98059, respectively. In the VSMCs of IMA, the connexin43 expression was markedly low and maintained at a reduced level even after 3 h stimulation. IGF-1 dose-dependently induced mRNA expression of connexin43 in the VSMCs of SV, which was blocked by PD98059. However, in VSMCs of IMA there was no significant effect of lGF-1 on the connexin43 mRNA expression. Conclusion. These data suggest that connexin43 expression can be influenced by Ang 11 and lGF-1 through ERK and p38 pathways and may contribute to the pathogenesis of vein graft disease following coronary artery bypass grafting. (c) 2007 Elsevier Inc. All rights reserved.
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