期刊
JOURNAL OF CELLULAR BIOCHEMISTRY
卷 112, 期 8, 页码 1978-1984出版社
WILEY-BLACKWELL
DOI: 10.1002/jcb.23169
关键词
CHOLINERGIC RECEPTORS; SURVIVAL SIGNALING; ENDOTHELIUM; APOPTOSIS; CORONARY ARTERY DISEASE
资金
- American Heart Association [SDG0635250N]
- University of Toledo College of Medicine
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [0951549] Funding Source: National Science Foundation
Nicotinic acetylcholine receptors (nAChRs) have recently emerged as critical players in modulation of endothelial function. In particular, studies on endothelial cells from different vascular beds have shown anti-apoptotic actions of nicotinic stimulation, but whether there is actually activation of survival signaling downstream nAChR function has not been explored. In the present work we used human coronary artery endothelial cells (HCAECs) and a pharmacological approach to examine the impact of cholinergic stimulation on survival signaling pathways. Our findings show that cholinergic receptors promote activation of three typical survival routes: the phosphatidyl-inositol-3-kinase (PI3K)/AKT axis, activated downstream muscarinic and nAChRs; the JAK2/STAT3 axis, activated downstream nAChR; and ERK1/2 MAP kinases, activated by both muscarinic acetylcholine receptor (mAChR) and nAChR. Based on their sensitivity to a-bungarotoxin, nicotinic regulation of JAK2/STAT3 and ERK1/2 occurs downstream alpha 7-nAChRs. The present findings suggest that in HCAECs the two cholinergic receptors may act concertedly to induce an efficient survival response of coronary cells when exposed to pro-apoptotic stimuli. J. Cell. Biochem. 112: 1978-1984, 2011. (C) 2011 Wiley-Liss, Inc.
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