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Heat Shock Protein 90 Inhibitor (17-AAG) Induces Apoptosis and Decreases Cell Migration/Motility of Keloid Fibroblasts

Authors
 Yun, In Sik ; Lee, Mi Hee ; Lee, Won Jai ; Park, Jong-Chul ; Lew, Dae Hyun ; Rah, Dong Kyun 
Citation
 Plastic and Reconstructive Surgery, Vol.136(1) : 44e~53e, 2015 
Journal Title
 Plastic and Reconstructive Surgery 
ISSN
 0032-1052 
Issue Date
2015
Abstract
BACKGROUND: The regulation of apoptosis, proliferation, and migration of fibroblasts is altered in keloids. The 90-kDa heat shock protein (heat shock protein 90) is known to play a key role in such regulation. Therefore, the authors investigated whether the inhibition of heat shock protein 90 in keloid fibroblasts could induce apoptosis and attenuate keloid fibroblast proliferation and migration. METHODS: The authors evaluated heat shock protein 90 expression in keloid tissues with immunohistochemistry. The authors used cell viability [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assays and annexin V/propidium iodide staining for apoptosis, a wound healing model and cell tracking system to assess cell migration, and Akt Western blotting analysis in keloid fibroblasts after inhibition of heat shock protein 90 with 17-allylaminodemethoxygeldanamycin (17-AAG). RESULTS: The expression of heat shock protein 90 in keloid tissues was significantly increased compared with normal tissues. The 17-AAG-treated keloid fibroblasts showed significantly decreased proliferation, promotion of apoptosis, and decreased expression of Akt. Furthermore, a dose-dependent decrease in cell migration was noted after 17-AAG treatment of keloid fibroblasts. The 17-AAG-treated keloid fibroblasts had less directionality to the wound center and migrated a shorter distance. CONCLUSIONS: The authors confirmed that the inhibition of heat shock protein 90 in keloid fibroblasts could promote apoptosis and attenuate proliferation and migration of keloid fibroblasts. Therefore, the authors think that the inhibition of heat shock protein 90 is a key factor in the regulation of biological processes in keloids. With further preclinical study, the authors will be able to apply these results clinically for keloid treatment.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/140490
DOI
10.1097/PRS.0000000000001362
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Dept. of Medical Engineering
1. 연구논문 > 1. College of Medicine > Dept. of Plastic Surgery & Reconstructive Surgery
Yonsei Authors
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Link
 http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00006534-201507000-00014&LSLINK=80&D=ovft
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