Role for heat shock protein 90? in the proliferation and migration of HaCaT cells and in the deep second-degree burn wound healing in mice.

ABSTRACT: Inflammation, proliferation, and tissue remodeling are essential steps for wound healing. The hypoxic wound microenvironment promotes cell migration through a hypoxia--heat shock protein 90 alpha (Hsp90?)--low density lipoprotein receptor-related protein-1 (LRP-1) autocrine loop. To elucidate the role of this autocrine loop on burn wound healing, we investigated the expression profile of Hsp90? at the edge of burn wounds and found a transient increase in both mRNA and protein levels. Experiments performed with a human keratinocyte cell line--HaCaT also confirmed above results. 17-dimethylaminoethylamino-17demethoxygeldanamycin hydrochloride (17-DMAG), an Hsp90? inhibitor, was used to further evaluate the function of Hsp90? in wound healing. Consistently, topical application of Hsp90? in the early stage of deep second-degree burn wounds led to reduced inflammation and increased tissue granulation, with a concomitant reduction in the size of the wound at each time point tested (p<0.05). Consequently, epidermal cells at the wound margin progressed more rapidly causing an expedited healing process. In conclusion, these results provided a rationale for the therapeutic effect of Hsp90? on the burn wound management.

SUBMITTER: Zhang Y 

PROVIDER: S-EPMC4128658 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature