Cytosolic Heat Shock Protein 60, Apoptosis, and Myocardial Injury

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Cytosolic heat shock protein 60, apoptosis, and myocardial injury.

BACKGROUND Heat shock proteins (HSPs) are well known for their ability to "protect" the structure and function of native macromolecules, particularly as they traffic across membranes. Considering the role of key mitochondrial proteins in apoptosis and the known antiapoptotic effects of HSP27 and HSP72, we postulated that HSP60, primarily a mitochondrial protein, also exerts an antiapoptotic eff...

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Cytosolic heat shock protein 60, hypoxia, and apoptosis.

BACKGROUND Heat shock protein (HSP)60 is an abundant protein found primarily in the mitochondria, though 15% to 20% is found in the cytosol. Previously we observed that HSP60 complexes with bax in the cytosol. Reduction in HSP60 precipitates translocation of bax to the mitochondria and apoptosis. We hypothesized that HSP60 would decrease with hypoxia/reoxygenation and that this would precipitat...

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S . R . Kirchhoff , S . Gupta and A . A . Knowlton Cytosolic Heat Shock Protein 60 , Apoptosis , and Myocardial Injury

Background—Heat shock proteins (HSPs) are well known for their ability to " protect " the structure and function of native macromolecules, particularly as they traffic across membranes. Considering the role of key mitochondrial proteins in apoptosis and the known antiapoptotic effects of HSP27 and HSP72, we postulated that HSP60, primarily a mitochondrial protein, also exerts an antiapoptotic e...

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Extracellular heat shock protein 60, cardiac myocytes, and apoptosis.

RATIONALE Previously, we have found that changes in the location of intracellular heat shock protein (HSP)60 are associated with apoptosis. HSP60 has been reported to be a ligand of toll-like receptor (TLR)-4. OBJECTIVE We hypothesized that extracellular HSP60 (exHSP60) would mediate apoptosis via TLR4. METHODS AND RESULTS Adult rat cardiac myocytes were treated with HSP60, either recombina...

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ژورنال

عنوان ژورنال: Circulation

سال: 2002

ISSN: 0009-7322,1524-4539

DOI: 10.1161/01.cir.0000019403.35847.23