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Carbachol inhibits TNF-alpha-induced endothelial barrier dysfunction through alpha 7 nicotinic receptors.

Authors: Li, YZ  Liu, XH  Rong, F  Hu, S  Sheng, ZY 
Citation: Li YZ, etal., Acta Pharmacol Sin. 2010 Oct;31(10):1389-94. Epub 2010 Sep 27.
Pubmed: (View Article at PubMed) PMID:20871620
DOI: Full-text: DOI:10.1038/aps.2010.165

AIM: To test whether carbachol can influence endothelial barrier dysfunction induced by tumor necrosis factor (TNF)-alpha and whether the alpha 7 nicotinic receptor can mediate this process. METHODS: Rat cardiac microvascular endothelial cells were exposed to carbachol followed by TNF-alpha treatment in the presence or the absence of alpha-bungarotoxin (an antagonist of the alpha 7 nicotinic receptor). Permeability of endothelial cells cultured on Transwell fi lters was assayed using FITC-albumin. F-actin was stained with FITC- phalloidin. Expression of vascular endothelial cadherin, intercellular adhesion molecule 1 (ICAM-1), phosphor-ERK1/2 and phosphor-JNK was detected using Western blot. RESULTS: Carbachol (2 mumol/L-2 mmol/L) prevented increase in endothelial cell permeability induced by TNF-alpha (500 ng/mL) in a dose-dependent manner. Further, it attenuated the down-regulation of vascular endothelial cadherin and the up-regulation of ICAM-1 induced by TNF-alpha. In addition, treatment of endothelial cells with carbachol decreased phosphor-ERK1/2 and phosphor-JNK. These effects of carbachol were blocked by alpha-bungarotoxin 3 mug/mL. CONCLUSION: These data suggest that the inhibitory effect of carbachol on TNF-alpha-induced endothelial barrier dysfunction mediated by the alpha 7 nicotinic receptor.


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RGD Object Information
RGD ID: 4145344
Created: 2010-11-01
Species: All species
Last Modified: 2010-11-01
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.