Extracellular Heat Shock Protein 60, Cardiac Myocytes, and Apoptosis

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...

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...

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...

Trophoblast Apoptosis through TLR4 Heat Shock Protein 60 Induces Chlamydia

Autophagy Protects Monocytes from Wolbachia Heat Shock Protein 60–Induced Apoptosis and Senescence

Monocyte dysfunction by filarial antigens has been a major mechanism underlying immune evasion following hyporesponsiveness during patent lymphatic filariasis. Recent studies have initiated a paradigm shift to comprehend the immunological interactions of Wolbachia and its antigens in inflammation, apoptosis, lymphocyte anergy, etc. Here we showed that recombinant Wolbachia heat shock protein 60...