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- Title
The upregulation of heat shock protein 47 in human gingival fibroblasts stimulated with cyclosporine A.
- Authors
Chang, T.‐Y.; Tsai, C.‐H.; Chang, Y.‐C.
- Abstract
Chang T-Y, Tsai C-H, Chang Y-C. The upregulation of heat shock protein 47 in human gingival fibroblasts stimulated with cyclosporine A. J Periodont Res 2010; 45: 317–322. © 2009 John Wiley & Sons A/S Background and Objective: Heat shock protein 47 (Hsp47), a collagen-specific molecular chaperone, is involved in the processing and/or secretion of procollagen. Heat shock protein 47 is consistently and dramatically upregulated in a variety of fibrotic diseases. The aim of this study was to compare Hsp47 expression in normal gingival tissues and cyclosporine A-induced gingival overgrowth specimens and further explore the potential mechanisms that may lead to induction of Hsp47 expression. Material and Methods: Fifteen cyclosporine A-induced gingival overgrowth specimens and five normal gingival tissues were examined by immunohistochemistry. Western blot was used to investigate the effects of cyclosporine A on the expression of Hsp47 in human gingival fibroblasts. In addition, Aggregatibacter actinomycetemcomitans, interleukin-1α (IL-1α) and mitogen-activated protein kinase kinase (MEK) inhibitor U0126 were added to seek the possible regulatory mechanisms of Hsp47 expression. Results: A significantly higher percentage of cells positively stained for Hsp47 was noted in the cyclosporine A-induced gingival overgrowth group than in the normal gingival group ( p < 0.05). Expression of Hsp47 was observed mainly in the cytoplasm of fibroblasts, endothelial cells, epithelial cells and inflammatory cells. Expression of Hsp47 was significantly higher in cyclosporine A-induced gingival overgrowth specimens with higher levels of inflammatory infiltrates ( p < 0.05). Cyclosporine A upregulated Hsp47 expression in human gingival fibroblasts in a dose-dependent manner ( p < 0.05). The addition of A. actinomycetemcomitans or interlukin-1α significantly increased Hsp47 expression compared with cyclosporine A alone ( p < 0.05). The MEK inhibitor U0126 was found to inhibit cyclosporine A-induced Hsp47 expression ( p < 0.05). Conclusion: Expression of Hsp47 is significantly upregulated in cyclosporine A-induced gingival overgrowth specimens, and Hsp47 expression induced by cyclosporine A in fibroblasts may be mediated by the MEK signal transduction pathway. The expression of Hsp47 could be significantly enhanced by A. actinomycetemcomitans and interlukin-1α.
- Subjects
CYCLOSPORINE; HEAT shock proteins; FIBROBLASTS; EXTRACELLULAR matrix proteins; IMMUNOHISTOCHEMISTRY
- Publication
Journal of Periodontal Research, 2010, Vol 45, Issue 3, p317
- ISSN
0022-3484
- Publication type
Article
- DOI
10.1111/j.1600-0765.2009.01238.x