Effect of heat shock proteins on survival of isolated aortic cells from normal and atherosclerotic cynomolgus macaques

Hsp70 and Its Molecular Role in Nervous System Diseases

“…It is now well known that Hsp70 can be released from some cells and taken up by others in a biologically active form [178, 180, 181]. Although there is no evidence on how Hsp70 works extracellularly, there is evidence that Hsp70 can be internalized and imported into the cytoplasm and nucleus of many cell types to promote cell survival [176, 182–187]. …”

“…Extracellular Hsp70 may, therefore, play a compensatory role after stress to promote survival, inhibit apoptosis, or both. The first observation of the stress tolerance-enhancing activity of exogenous Hsc/Hsp70 was reported by Johnson and coworkers, who showed that Hsc/Hsp70 added to the culture medium in vitro can bind to arterial smooth muscle cells and improve their resistance to nutrient-deprivation stress [182, 183]. A protective effect was also observed in cultured monocytes [184].…”

Circulating Heat Shock Protein 70 in Health, Aging and Disease

“…Hsp can be secreted by viable cells, such as peripheral blood mononuclear cells which are thought to contribute significantly to circulating Hsp70 [5,6]. Extracellular Hsp have been reported to exhibit beneficial properties, such as enhancing the survival of cultured cells [7], and mitigating autoimmune disorders [8-10]. The prevention or arrest of inflammatory damage by Hsp is thought to involve T cell reactivity, resulting in the enhancement and/or mitigation of specific cytokine profiles [8,11,12].…”

The atheroprotective properties of Hsp70: a role for Hsp70-endothelial interactions?

“…Hsp70 prevents caspase-3 and SAPK/JNK activation in heat-shock-or ceramide-induced apoptosis (Mosser et al 1997;Ahn et al 1999). Although the cytoprotective effects of intracellular Hsp70 are established (Jäättelä et al 1992;Simon et al 1995;Samali and Cotter 1996;Lasunskaia et al 1997;Mosser et al 1997), exogenous Hsp70 protects heat-stressed cynomolgus macaque aortic cells (Johnson et al 1990) and serum-deprived rabbit arterial smooth muscle cells (Johnson and Tytell 1993), the latter by a mechanism which involves cell association but not internalisation. The mechanism by which such protection is afforded is currently unknown, and the cell surface interactions involved have not been identified.…”