autoantibodies targeting at1 receptor from patients with acute coronary syndrome upregulate proinflammatory cytokines expression in endothelial cells involving nf-κb pathway

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ID: 145620
2014
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Abstract
Our study intended to prove whether agonistic autoantibodies to angiotensin II type 1 receptor (AT1-AAs) exist in patients with coronary heart disease (CHD) and affect the human endothelial cell (HEC) by upregulating proinflammatory cytokines expression involved in NF-κB pathway. Antibodies were determined by chronotropic responses of cultured neonatal rat cardiomyocytes coupled with receptor-specific antagonists (valsartan and AT1-EC2) as described previously. Interleukin-6 (IL-6), vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemotactic protein-1 (MCP-1) expression were improved at both mRNA and protein levels in HEC, while NF-κB in the DNA level was improved detected by electrophoretic mobility shift assays (EMSA). These improvements could be inhibited by specific AT1 receptor blocker valsartan, NF-κB blocker pyrrolidine dithiocarbamate (PDTC), and specific short peptides from the second extracellular loop of AT1 receptor. These results suggested that AT1-AAs, via the AT1 receptor, induce expression of proinflammatory cytokines involved in the activation of NF-κB. AT1-AAs may play a great role in the pathogenesis of the acute coronary syndrome by mediating vascular inflammatory effects involved in the NF-κB pathway.
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Authors Weijuan Li, Zhi Li, Yaoqi Chen, Songhai Li, Yuanyuan Lv, Wenping Zhou, Mengyang Liao, Feng Zhu, Zihua Zhou, Xiang Cheng, Qiutang Zeng, Yuhua Liao, Yumiao Wei
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Journal journal of photochemistry and photobiology b, biology
Year 2014
DOI
10.1155/2014/342693
URL
http://dx.doi.org/10.1155/2014/342693
Keywords
immunologic diseases allergy

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