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Mortalin deficiency suppresses fibrosis and induces apoptosis in keloid spheroids

Authors
 Won Jai Lee  ;  Hyo Min Ahn  ;  Youjin Na  ;  Renu Wadhwa  ;  JinWoo Hong  ;  Chae-Ok Yun 
Citation
 Scientific Reports, Vol.7(1) : 12957, 2017 
Journal Title
 Scientific Reports 
Issue Date
2017
Abstract
Mortalin (Mot) is a mitochondrial chaperone of the heat shock protein 70 family and it's pro-proliferative and anti-apoptosis functions could be associated with keloid pathogenesis, and blocking of mortalin and its interaction with p53 might be a potential novel target for the treatment of keloid. Therefore, we generated mortalin-specific small hairpin (sh) RNAs (dE1-RGD/GFP/shMot) and introduced into keloid spheroids for examination of its apoptotic and anti-fibrotic effect. On keloid tissues, mortalin expression was higher than adjacent normal tissues and it's protein expressions were activated keloid fibroblasts (KFs). After primary keloid spheroid were transduced with dE1-RGD/GFP/shMot for knockdown of mortalin, expression of type I, III collagen, fibronectin, and elastin was significantly reduced and transforming growth factor-β1, epidermal growth factor receptor (EGFR), Extracellular Signal-Regulated Kinases 1 and 2 (Erk 1/2), and Smad 2/3 complex protein expression were decreased. In addition, increased TUNEL activities and cytochrome C were observed. Further, for examine of mortalin and p53 interaction, we performed immunofluorescence analysis. Knockdown of mortalin relocated p53 to the cell nucleus in primary keloid spheroids by dE1-RGD/GFP/shMot transduction. These results support the utility of knockdown of mortalin to induce apoptosis and reduce ECMs expression in keloid spheroid, which may be highly beneficial in treating keloids.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/161076
DOI
10.1038/s41598-017-13485-y
Appears in Collections:
1. Journal Papers (연구논문) > 1. College of Medicine (의과대학) > Dept. of Plastic and Reconstructive Surgery (성형외과학교실)
Yonsei Authors
이원재(Lee, Won Jai)
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