The Effect Of Acute Hypoxia On Heat Shock Protein 72 Expression And Oxidative Stress In Vivo

2010 ◽  
Vol 42 ◽  
pp. 466
Author(s):  
Lee Taylor ◽  
Adrian W. Midgley ◽  
Bryna CR Chrismas ◽  
Leigh A. Madden ◽  
Rebecca V. Vince ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Acute Hypoxia ◽  
Heat Shock Protein 72 ◽  
And Oxidative Stress

The effect of acute hypoxia on heat shock protein 72 expression and oxidative stress in vivo

2010 ◽  
Vol 109 (5) ◽  
pp. 849-855 ◽  
Author(s):  
Lee Taylor ◽  
Adrian W. Midgley ◽  
Bryna Chrismas ◽  
Leigh A. Madden ◽  
Rebecca V. Vince ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Acute Hypoxia ◽  
Heat Shock Protein 72 ◽  
And Oxidative Stress

scholarly journals Heat shock protein 72 regulates hepatic lipid accumulation

2018 ◽  
Vol 315 (4) ◽  
pp. R696-R707 ◽  
Author(s):  
Ashley E. Archer ◽  
Robert S. Rogers ◽  
Alex T. Von Schulze ◽  
Joshua L. Wheatley ◽  
E. Matthew Morris ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Heat Shock ◽  
Glucose Tolerance ◽  
Heat Shock Protein ◽  
Lipid Accumulation ◽  
Acid Oxidation ◽  
Mitochondrial Morphology ◽  
Primary Hepatocytes ◽  
Heat Shock Protein 72

Induction of the chaperone heat shock protein 72 (HSP72) through heat treatment (HT), exercise, or overexpression improves glucose tolerance and mitochondrial function in skeletal muscle. Less is known about HSP72 function in the liver where lipid accumulation can result in insulin resistance and nonalcoholic fatty liver disease (NAFLD). The purpose of this study was 1) to determine whether weekly in vivo HT induces hepatic HSP72 and improves glucose tolerance in rats fed a high-fat diet (HFD) and 2) to determine the ability of HSP72 to protect against lipid accumulation and mitochondrial dysfunction in primary hepatocytes. Male Wistar rats were fed an HFD for 15 wk and were given weekly HT (41°C, 20 min) or sham treatments (37°C, 20 min) for the final 7 wk. Glucose tolerance and insulin sensitivity were assessed, along with HSP72 induction and triglyceride storage, in the skeletal muscle and liver. The effect of an acute loss of HSP72 in primary hepatocytes was examined via siRNA. Weekly in vivo HT improved glucose tolerance, elevated muscle and hepatic HSP72 protein content, and reduced muscle triglyceride storage. In primary hepatocytes, mitochondrial morphology was changed, and fatty acid oxidation was reduced in small interfering HSP72 (siHSP72)-treated hepatocytes. Lipid accumulation following palmitate treatment was increased in siHSP72-treated hepatocytes. These data suggest that HT may improve systemic metabolism via induction of hepatic HSP72. Additionally, acute loss of HSP72 in primary hepatocytes impacts mitochondrial health as well as fat oxidation and storage. These findings suggest therapies targeting HSP72 in the liver may prevent NAFLD.

scholarly journals Exercise induces the release of heat shock protein 72 from the human brain in vivo

2004 ◽  
Vol 9 (3) ◽  
pp. 276 ◽  
Author(s):  
G. I. Lancaster ◽  
K. Møller ◽  
B. Nielsen ◽  
N. H. Secher ◽  
M. A. Febbraio ◽  
...  
Keyword(s):  
Heat Shock ◽  
Heat Shock Protein ◽  
Human Brain ◽  
Heat Shock Protein 72

scholarly journals Spironolactone reduces oxidative stress in living donor kidney transplantation: a randomized controlled trial

2019 ◽  
Vol 317 (3) ◽  
pp. F519-F528 ◽  
Author(s):  
Luis Eduardo Morales-Buenrostro ◽  
Juan Antonio Ortega-Trejo ◽  
Rosalba Pérez-Villalva ◽  
Lluvia A. Marino ◽  
Yvett González-Bobadilla ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Kidney Function ◽  
Living Donor ◽  
Treated Group ◽  
Lipocalin 2 ◽  
Heat Shock Protein 72 ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Neutrophil Gelatinase

Mineralocorticoid receptor antagonism prevents acute kidney injury induced by ischemia-reperfusion in rodent and pig preclinical models. In a pilot study, we showed that spironolactone (25 mg) reduced oxidative stress after 5 days of kidney transplant (KT). In the present study, we investigated the effects of higher doses (50 and 100 mg) of spironolactone on kidney function, tubular injury markers, and oxidative stress in living donor KT recipients. We included KT recipients aged 18 yr or older who received immunosuppression therapy with IL-2 receptor antagonist, mycophenolate mofetil, corticosteroids, and tacrolimus with negative cross-match, and compatible blood group. Patients were randomized to receive placebo ( n = 27), spironolactone (50 mg, n = 25), or spironolactone (100 mg, n = 25). Treatment was given from 3 days before and up to 5 days after KT. Serum creatinine, K+, urine neutrophil gelatinase-associated lipocalin-2, heat shock protein 72, and 8-hydroxy-2-deoxyguanosine levels were assessed. As expected, kidney function was improved after KT. Serum K+ remained in the normal range along the study. There was no significant effect of spironolactone on urinary neutrophil gelatinase-associated lipocalin-2 levels, whereas the increase in urinary heat shock protein 72 levels tended to be less intense in the 100 mg spironolactone-treated group ( P = 0.054). In the placebo-treated group, urinary 8-hydroxylated-guanosine levels increased on days 3 and 5 after transplantation. This effect was prevented in patients that received spironolactone. In conclusion, spironolactone reduces the acute increase in urinary oxidative stress in living donor KT recipients.

Overexpression of Heat Shock Protein 72 in Transgenic Mice Decreases Infarct Size In Vivo

Circulation ◽  
1996 ◽  
Vol 94 (6) ◽  
pp. 1408-1411 ◽  
Author(s):  
Jonathan J. Hutter ◽  
Ruben Mestril ◽  
Eunice K.W. Tam ◽  
Richard E. Sievers ◽  
Wolfgang H. Dillmann ◽  
...  
Keyword(s):  
Heat Shock ◽  
Transgenic Mice ◽  
Heat Shock Protein ◽  
Infarct Size ◽  
Heat Shock Protein 72

scholarly journals Thermal Treatment Attenuates Neointimal Thickening With Enhanced Expression of Heat-Shock Protein 72 and Suppression of Oxidative Stress

Circulation ◽  
2004 ◽  
Vol 109 (14) ◽  
pp. 1763-1768 ◽  
Author(s):  
Motoi Okada ◽  
Naoyuki Hasebe ◽  
Yoshiaki Aizawa ◽  
Kazuma Izawa ◽  
Jun-ichi Kawabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Thermal Treatment ◽  
Heat Shock Protein ◽  
Heat Shock Protein 72 ◽  
Neointimal Thickening ◽  
Enhanced Expression

Acute and severe hypobaric hypoxia increases oxidative stress and impairs mitochondrial function in mouse skeletal muscle

2005 ◽  
Vol 99 (4) ◽  
pp. 1247-1253 ◽  
Author(s):  
José Magalhães ◽  
António Ascensão ◽  
José M. C. Soares ◽  
Rita Ferreira ◽  
Maria J. Neuparth ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Vitamin E ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Hypobaric Hypoxia ◽  
Sulfhydryl Group ◽  
Protein Carbonyls ◽  
Heat Shock Protein 60

Severe high-altitude hypoxia exposure is considered a triggering stimulus for redox disturbances at distinct levels of cellular organization. The effect of an in vivo acute and severe hypobaric hypoxic insult (48 h at a pressure equivalent to 8,500 m) on oxidative damage and respiratory function was analyzed in skeletal muscle mitochondria isolated from vitamin E-supplemented (60 mg/kg ip, 3 times/wk for 3 wk) and nonsupplemented mice. Forty male mice were randomly divided into four groups: control + placebo, hypoxia + placebo (H + P), control + vitamin E, and hypoxia + vitamin E. Significant increases in mitochondrial heat shock protein 60 expression and protein carbonyls group levels and decreases in aconitase activity and sulfhydryl group content were found in the H + P group when compared with the control + placebo group. Mitochondrial respiration was significantly impaired in animals from the H + P group, as demonstrated by decreased state 3 respiratory control ratio and ADP-to-oxygen ratio and by increased state 4 with both complex I- and II-linked substrates. Using malate + pyruvate as substrates, hypoxia decreased the respiratory rate in the presence of carbonyl cyanide m-chlorophenylhydrazone and also stimulated oligomycin-inhibited respiration. However, vitamin E treatment attenuated the effect of hypoxia on the mitochondrial levels of heat shock protein 60 and markers of oxidative stress. Vitamin E was also able to prevent most mitochondrial alterations induced by hypobaric hypoxia. In conclusion, hypobaric hypoxia increases mitochondrial oxidative stress while decreasing mitochondrial capacity for oxidative phosphorylation. Vitamin E was an effective preventive agent, which further supports the oxidative character of mitochondrial dysfunction induced by hypoxia.

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