Heat-Shock Protein 27 Induction and Redistribution During Re-Organization of the Actin Cytoskeleton After Renal Ischemia. • 1636

Abstract

Increasing evidence supports a regulatory role for HSP-27 in actin dynamics. Since cytoskeletal disruption is integral to ischemic renal injury, we evaluated expression and intracellular distribution of HSP-27 in rat renal cortex after 45 min of renal ischemia. HSP-27 was constitutively expressed, increased at 15 min reflow and peaked by 6 h reflow (3.6 fold baseline, p<0.05). Under control conditions, 80% of HSP-27 was distributed to the detergent soluble extracts; ischemia caused a shift of HSP-27 into the insoluble cytoskeletal fraction (to 50% of total, p<0.05). At 2 and 6 h reflow, HSP-27 redistributed into the soluble fraction. In control, HSP-27 was predominantly localized in a subapical distribution, a pattern intermediate between that of DNase reactive and microfilamentous actin. After ischemia, HSP-27 was localized throughout the cytoplasm in a pattern with small punctate accumulations similar to DNase reactive actin. During later reflow, HSP-27, DNase reactive and microfilamentous actin were all found in coarse intracytoplasmatic accumulations, and HSP-27 and microfilamentous actin re-accumulated in the subapical domain. Thus the temporal and spatial patterns of HSP-27 induction, distribution and intracellular localization strongly suggests specific interactions between HSP-27 and actin during the postischemic re-organization of the cytoskeleton.