Abrupt reoxygenation following hypoxia reduces electrical coupling between endothelial cells of wild-type but not connexin40 null mice in oxidant- and PKA-dependent manner Michael L. Bolon * ,† , Yves Ouellette ‡ , Fuyan Li * ,§ and Karel Tyml * ,† ,§ ,1 * Lawson Health Research Institute, London, Ontario, Canada; † Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada; ‡ Department of Pediatrics, Mayo Clinic College of Medicine, Rochester, Minnesota, USA; and § Department of Medical Biophysics, University of Western Ontario, London, Ontario, Canada 1 Correspondence: Lawson Health Research Institute, The Centre for Critical Illness Research, Victoria Research Laboratory, 6th Floor, 800 Commissioners Rd., East London, Ontario N6C 2V5, Canada. E-mail: ktyml@lhsc.on.ca <h3>SPECIFIC AIMS</h3> Electrical coupling between cells of the vascular wall plays a key role in control of vascular resistance. We aimed to determine the pathophysiological effect of hypoxia and reoxygenation (H/R) on this coupling, the signaling pathway, and its target protein in a model of cultured microvascular endothelial cells (EC) monolayers derived from mouse skeletal muscle. We focused on the role of the gap junction protein connexin 40 (Cx40), as well as H/R-induced reactive oxygen species (ROS) formation and protein kinase
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Abrupt reoxygenation following hypoxia reduces electrical coupling between endothelial cells of wild-type but not connexin40 null mice in oxidant- and PKA-dependent manner
Bolon, Michael L.; Ouellette, Yves; Li, Fuyan; Tyml, Karel
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, Volume 19 (12): 1725
Fed of American Socs for Experimental Biology – Oct 1, 2005
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