期刊
FEBS LETTERS
卷 582, 期 29, 页码 4039-4046出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2008.10.043
关键词
Gap junction; Gap junction intercellular communication; G-protein coupled receptors; Thrombin; Endothelin-1; ZO-1
资金
- NIH
- National Institute of General Medical Sciences [GM-55725]
- Bioengineering and Bioscience 2020 Funds
During the inflammatory response, activation of G-protein coupled receptors (GPCRs) by inflammatory mediators rapidly leads to inhibition of gap junction intercellular communication (GJIC); however, the steps that lead to this inhibition are not known. Combining high-resolution fluorescence microscopy and functional assays, we found that activation of the GPCRs PAR-1 and ET(A/B) by their natural inflammatory mediator agonists, thrombin and endothelin-1, resulted in rapid and acute internalization of gap junctions (GJs) that coincided with the inhibition of GJIC followed by increased vascular permeability. The endocytosis protein clathrin and the scaffold protein ZO-1 appeared to be involved in GJ internalization, and ZO-1 was partially displaced from GJs during the internalization process. These findings demonstrate that GJ internalization is an efficient mechanism for modulating GJIC in inflammatory response. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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