Adrenomedullin protects rat cerebral endothelial cells from oxidant damage in vitro.
Increased permeability and reduced cerebral endothelial cell (CEC) viability induced by oxidative stress are the hallmarks of the blood-brain barrier disruption. In our experiments hydrogen peroxide (H2O2, 0.5 mM) induced a continuous decrease of the transendothelial electrical resistance (TEER) and resulted in intercellular gap formations in cultured rat CECs. Adrenomedullin (AM) increased TEER, enhanced peripheral localization of F-actin bands and attenuated the increased permeability induced by H2O2. Furthermore, AM treatment preserved mitochondrial membrane potential, attenuated cytochrome c release, and consequently improved CEC viability in H2O2 treated cultures. These results suggest that AM treatment protects CECs against oxidative injury.
Chen
Lei
L
Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Iseigaoka 1-1, Yahatanishi-ku, Kitakyushu 807-8555, Japan.
Kis
Bela
B
Busija
David W
DW
Yamashita
Hiroshi
H
Ueta
Yoichi
Y
D000199:Actins / Q000378:metabolism; D053607:Adrenomedullin; D000818:Animals; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism; D002470:Cell Survival; D002478:Cells, Cultured; D045304:Cytochromes c / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000166:cytology*; D006861:Hydrogen Peroxide / Q000378:metabolism / Q000494:pharmacology; D008564:Membrane Potentials; D008856:Microscopy, Fluorescence; D008928:Mitochondria / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D010455:Peptides / Q000378:metabolism / Q000494:pharmacology*; D010539:Permeability; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury; D013687:Telencephalon / Q000166:cytology*; D013997:Time Factors
D000199:Actins; D016877:Oxidants; D010455:Peptides; D053607:Adrenomedullin; D045304:Cytochromes c; D006861:Hydrogen Peroxide