0 169

Cited 0 times in

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

Authors
 Yun, In Sik  ;  Lee, Mi Hee  ;  Rah, Dong Kyun  ;  Lew, Dae Hyun  ;  Park, Jong-Chul  ;  Lee, Won Jai 
Citation
 Plastic and Reconstructive Surgery, Vol.136(1) : 44-53, 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
https://ir.ymlib.yonsei.ac.kr/handle/22282913/140490
DOI
10.1097/PRS.0000000000001362
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Medical Engineering (의학공학교실)
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Plastic and Reconstructive Surgery (성형외과학교실)
Yonsei Authors
나동균(Rah, Dong Kyun) ; 박종철(Park, Jong Chul) ; 유대현(Lew, Dae Hyun) ; 윤인식(Yun, In Sik) ; 이미희(Lee, Mi Hee) ; 이원재(Lee, Won Jai)
사서에게 알리기
  feedback
Full Text
http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00006534-201507000-00014&LSLINK=80&D=ovft
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse