scholarly journals Heat shock protein 72 expression is not essential for exercise induced protection against infarction and apoptosis following ischemia‐reperfusion

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
John C Quindry ◽  
Karyn L Hamilton ◽  
Joel P French ◽  
Youngil Lee ◽  
Zsolt Murlasits ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Ischemia Reperfusion ◽  
Heat Shock Protein 72 ◽  
Exercise Induced

scholarly journals L-NAME Treatment Enhances Exercise-induced Content of Myocardial Heat Shock Protein 72 (Hsp72) in Rats

2011 ◽  
Vol 27 (5) ◽  
pp. 479-486 ◽  
Author(s):  
Wellington Lunz ◽  
Luciano S.A. Capettini ◽  
Ana P.C. Davel ◽  
Carolina D. Munhoz ◽  
Josiane F. da Silva ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Heat Shock Protein 72 ◽  
Exercise Induced

scholarly journals Heat Shock Protein 72 Enhances Manganese Superoxide Dismutase Activity During Myocardial Ischemia-Reperfusion Injury, Associated With Mitochondrial Protection and Apoptosis Reduction

Circulation ◽  
2002 ◽  
Vol 106 (12_suppl_1) ◽  
Author(s):  
Ken Suzuki ◽  
Bari Murtuza ◽  
Ivan A. Sammut ◽  
Najma Latif ◽  
Jay Jayakumar ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Reperfusion Injury ◽  
Manganese Superoxide Dismutase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Heat Shock Protein 72 ◽  
Manganese Superoxide

Background Heat shock protein 72 (HSP72) is known to provide myocardial protection against ischemia-reperfusion injury by its chaperoning function. Target molecules of this effect are presumed to include not only structural proteins but also other self-preservation proteins. The details, however, remain unknown. Manganese superoxide dismutase (Mn-SOD) is an enzyme that preserves mitochondria, a key organelle for cellular respiration, from reperfusion injury and limits mitochondria-related apoptosis. We hypothesized that Mn-SOD would play a role in HSP72-mediated cardioprotection. Methods and Results Rat hearts were transfected with human HSP72 by intra-coronary infusion of Hemagglutinating Virus of Japan-liposome, resulting in global myocardial overexpression of HSP72. After ischemia-reperfusion injury, cardiac function (left ventricular systolic pressure, maximum dP/dt, minimum dP/dt, and coronary flow) was improved in the HSP72-transfected hearts compared with control-transfected ones, corresponding with less leakage of creatine kinase and mitochondrial aspartate aminotransferase. Postischemic Mn-SOD content and activity in the HSP72-transfected hearts were enhanced in comparison with the controls (content: 96.9±4.1 versus 85.5±2.5% to the preischemic level, P =0.038; activity: 93.9±2.2 versus 82.2±3.7%, P =0.022), associated with improved mitochondrial respiratory function (postischemic percent respiratory control index; NAD + -linked: 81.3±3.8 versus 18.5±4.4%; FAD-linked: 71.8±5.5 versus 20.7±5.3%, P <0.001). In addition, incidence of postischemic cardiomyocyte apoptosis was attenuated in the HSP72-transfected hearts (4.0±1.1 versus 10.3±3.3%, P =0.036), correlating with an increased Bcl-2 level and reduced up-regulation of caspase-3. Conclusions These data suggest that the enhanced Mn-SOD activity during ischemia-reperfusion injury, which is associated with mitochondrial protection and apoptosis reduction, is a possible mechanism of HSP72-induced cardioprotection.

Effect of exercise with and without a thermal clamp on the plasma heat shock protein 72 response

2007 ◽  
Vol 103 (4) ◽  
pp. 1251-1256 ◽  
Author(s):  
Martin Whitham ◽  
Stewart J. Laing ◽  
Anna Jackson ◽  
Norbert Maassen ◽  
Neil P. Walsh
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Water Immersion ◽  
Passive Heating ◽  
Heat Shock Protein 72 ◽  
Catecholamine Response ◽  
Related Stress ◽  
Exercise Induced ◽  
Independent Effects ◽  
And Control

The contribution of heat and exercise related stress to the release of heat shock protein 72 (HSP72) is currently unknown. The purpose of the present study was to determine the combined and independent effects of heat and exercise on the extracellular (e)HSP72 response. Eleven moderately trained male volunteers [means ± SD: age 21 ± 4 yr; body mass 75.7 ± 7.7 kg; maximal oxygen uptake (V̇o2 max) 57.8 ± 3.3 ml·kg−1·min−1] completed four 2-h, heat-manipulated, water-immersion trials. Trials were exercise-induced heat (EIH; rectal temperature change +2.2°C), clamped exercise (CEx; 0°C), passive heating (PHT; +2.3°C), and control (Con; 0°C). Exercise trials (EIH and CEx) comprised deep-water running at 58.5 ± 2.4 and 59.1 ± 1.7% v̇o2max. eHSP72 and catecholamine concentrations were determined by ELISA and HPLC, respectively, pre- and postimmersion. All trials induced an eHSP72 response ( P < 0.05) with postimmersion values significantly greater on EIH compared with other trials (6.0 ± 3.4; CEx 3.8 ± 2.6; PHT 2.7 ± 2.1; Con 2.2 ± 1.9 ng/ml). Exercising with a thermal clamp blunted the eHSP72 response, but postimmersion values were also greater than Con. PHT induced a large catecholamine response, but postimmersion eHSP72 values did not reach significance vs. Con. Given that exercising with a thermal clamp evoked a significant increase in plasma eHSP72 concentration, exercise-related stressors other than heat appeared influential in stimulating HSP72 release. Moreover, the catecholamine data from PHT suggest neither epinephrine nor norepinephrine was solely responsible for eHSP72 release.

scholarly journals Attenuation of exercise-induced heat shock protein 72 expression blunts improvements in whole-body insulin resistance in rats with type 2 diabetes

2017 ◽  
Vol 22 (2) ◽  
pp. 263-269 ◽  
Author(s):  
Takamasa Tsuzuki ◽  
Hiroyuki Kobayashi ◽  
Toshinori Yoshihara ◽  
Ryo Kakigi ◽  
Noriko Ichinoseki-Sekine ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Whole Body ◽  
Heat Shock Protein 72 ◽  
Exercise Induced

scholarly journals Adrenomedullin Improves Cardiac Expression of Heat-Shock Protein 72 and Tolerance against Ischemia/Reperfusion Injury in Insulin-Resistant Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (3) ◽  
pp. 1450-1455 ◽  
Author(s):  
Yasuko Torigoe ◽  
Naohiko Takahashi ◽  
Masahide Hara ◽  
Hironobu Yoshimatsu ◽  
Tetsunori Saikawa
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heat Shock Protein 72 ◽  
Insulin Resistant
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