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Critical role of EP2-PKA signaling reduced myocardial function via macrophages activation

 
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Research Article  
dx.doi.org/10.18081/2333-5106/015-12/780-792
American Journal of BioMedicine Volume 3, Issue 12, pages 780-792
Received: July 23, 2015; accepted: October 30, 2015; published: December 19, 2015


Carmen S. Bootha, Hashimoto G. Weisa, b, Pablo Halesa, Amanda H. Matherlya, Lynn C. Grafa mail of corresponding author

Abstract

Upon tissue damage or infection, monocytes are rapidly recruited to the tissue, where they differentiate into tissue macrophages. Macrophages are remarkably plastic and can change their functional phenotype depending on the environmental cues they receive. TLR ligation is prostaglandin E2 (PGE2), which is well known to increase intracellular cAMP upon G protein-coupled receptor ligation. This study explored EP2-PKA regulation in mice myocardial macrophages stimulated with the TLR4 and cardio-protective role of  EP2-PKA suppression. The data showed that the LPS-activated macrophage-mediated cardiotoxicity was completely abolished in both in vitro and in vivo lacking macrophage EP2.

Keywords: Macrophages; EP2-PKA; Cardio-protective; TLR ligation

Copyright © 2015 by The American Society for BioMedicine and BM-Publisher, Inc.

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