Prostaglandins Mediate the Expression of a 72-kDa Heat Shock Protein in Human Fibroblasts

Abstract

Highly conserved heat shock proteins (HSPs) function to maintain cellular homeostasis during stress [1]. At least in part, preservation by HSPs of cellular functions is achieved through protein refolding and degradation and export of damaged proteins [2] HSPs of different molecular weights are induced by various stimuli, including elevated temperatures, oxygen free radicals, tissue trauma caused by ischemia and reperfusion, inhibitors of energy metabolism, cytokines, and infectious microoganisms [1, 3]. Recently, immunological functions of HSPs in intracellular processing, membrane anchoring, and presentation of antigens have been suggested [4, 5]. Previous studies from this laboratory have focused on the induction of HSP expression in association with autoimmunity [6]. Prostaglandins and other inflammatory products are released locally by cells involved in immune reactions [7]. The purpose of this study was to determine whether prostaglandins may participate as mediators in the expression of a 72-kDa HSP (HSP 72) in cultured human fibroblasts.