Phosphatase inhibitors prevent HSP27 dephosphorylation, destruction of stress fibrils, and morphological changes in endothelial cells during ATP depletion.
Pretreatment with phosphatase inhibitors did not affect the decrease in ATP content in endothelial cells, but inhibited HSP27 dephosphorylation and redistribution, damages to actin cytoskeleton, and morphological changes in cells. Our results suggest that inhibition of stress-induced HSP27 dephosphorylation protects cells from ischemia-induced damages.
Loktionova
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Laboratory of Cell Adhesion, Institute of Experimental Cardiology, Russian Research-and-Production Cardiology Complex, Russian Ministry of Health, Moscow. calab@cardio.ru
Kabakov
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AE
D000199:Actins / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism*; D001011:Aorta / Q000166:cytology; D002193:Cantharidin / Q000494:pharmacology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D055551:HSP27 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D006801:Humans; D008856:Microscopy, Fluorescence; D018832:Molecular Chaperones; D009363:Neoplasm Proteins / Q000378:metabolism*; D019319:Okadaic Acid / Q000494:pharmacology; D010744:Phosphoric Monoester Hydrolases / Q000037:antagonists & inhibitors; D010766:Phosphorylation; D020033:Protein Isoforms; D022502:Stress Fibers / Q000378:metabolism; D013997:Time Factors; D014471:Umbilical Veins / Q000166:cytology
D000199:Actins; D004791:Enzyme Inhibitors; D055551:HSP27 Heat-Shock Proteins; C057725:HSPB1 protein, human; D006360:Heat-Shock Proteins; D018832:Molecular Chaperones; D009363:Neoplasm Proteins; D020033:Protein Isoforms; D019319:Okadaic Acid; D000255:Adenosine Triphosphate; D010744:Phosphoric Monoester Hydrolases; D002193:Cantharidin