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Heat‐shock protein expression in canine corneal wound healing
Author(s) -
Peterson Cornelia W. M.,
Carter Renee T.,
Bentley Ellison,
Murphy Christopher J.,
Chandler Heather L.
Publication year - 2016
Publication title -
veterinary ophthalmology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.594
H-Index - 50
eISSN - 1463-5224
pISSN - 1463-5216
DOI - 10.1111/vop.12302
Subject(s) - cornea , wound healing , hsp70 , stromal cell , immunohistochemistry , heat shock protein , biology , pathology , corneal epithelium , stroma , epithelium , hsp27 , ex vivo , in vivo , immunology , medicine , gene , biochemistry , microbiology and biotechnology , neuroscience
Objective Heat‐shock proteins, particularly the 70‐ kD a member (Hsp70), have been implicated in facilitating wound healing in multiple tissues. Expression and localization of three HSP s were assessed in normal and wounded canine corneas to elucidate a role in epithelial healing. Methods Paraffin‐embedded normal corneas, acute and repeatedly abraded corneas, and keratectomies of spontaneous chronic corneal epithelial defects ( SCCED s) were subjected to routine immunohistochemistry for Hsp27, 47, and 70 expression. Ex vivo corneal defects were created and treated with anti‐ HSP s or IgG controls, and wound healing was monitored. Primary cultures of canine corneal stromal fibroblasts and corneal epithelial cells were treated with exogenous Hsp70, and an artificial wound was created in vitro to monitor restoration of the monolayer. Results Normal canine corneas exhibited constitutive expression of all HSP s evaluated. Inducible expression was demonstrated in acutely wounded tissues, and expression in the chronically abraded corneas was relocalized. All HSP expression was below the limits of detection in the epithelium of SCCED samples. Inhibition of HSP s in culture resulted in delayed wound healing when compared to controls. Hsp70‐treated fibroblasts demonstrated significantly ( P < 0.001) increased migration and proliferation compared to the vehicle control; however, there was no significant effect of exogenous Hsp70 on corneal epithelial cells. Conclusions These findings suggest that HSP s are induced in the normal canine cornea during re‐epithelialization. Hsp70 expression is likely important for inducing the cytoarchitectural remodeling, migration, and proliferation necessary early in the canine corneal healing response, and suppressed expression may contribute to the pathophysiology of nonhealing defects.