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Salvatore Salomone
Catania University, Catania, Italy
Jean-Christophe Plumier
Université de Liège, Liège, Belgium
Series: Human Anatomy and Physiology, Cell Biology Research Progress
BISAC: SCI056000
Heat shock-mediated delayed protection against myocardial and cerebral ischemia has been attributed to induction of heat shock proteins (HSP), especially HSP70, in myocytesand neurons. However, heat shock preconditioning only induces HSP70 in endothelium. The purpose of this study was to examine the effect of heat shock on endothelium-dependent vasomotor tone. This book concludes that heat shock decreases vasomotor responses to vasoconstrictors by enhancing eNOS basal activity, through interaction with HSP70, that is robustly induced. Such an increase of eNOS might be related to protective effect of heat shock against ischemia reported in vivo. Finally, interaction between HSP70 and eNOS opens the intriguing possibility that HSP70 could have vasoregulatory properties in addition to its cytoprotective functions. (Imprint: Nova)
Table of Contents
Preface
Abstract
Introduction
Methods
Results
Heat Shock Effect on Vascular Tone Was Mediated by Endothelial Nitric Oxide Synthase (eNOS)
Stress Response Induction Increased the Expression of Heat Shock Proteins but Not of Nitric Oxide Synthase Isoforms
Inhibition of HSP90 Did Not Inhibitthe Effect Heat Shock on Phenylephrine-Induced Vasoconstriction
HSP70 Interacts with eNOS after Heat Shock
Discussion
References
Index
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