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タイトル: | HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloid Development |
著者: | Yamawaki, Satoko Naitoh, Motoko Kubota, Hiroshi Aya, Rino Katayama, Yasuhiro https://orcid.org/0000-0003-1218-9130 (unconfirmed) Ishiko, Toshihiro Tamura, Taku Yoshikawa, Katsuhiro Enoshiri, Tatsuki Ikeda, Mika Suzuki, Shigehiko |
著者名の別形: | 内藤, 素子 綾, 梨乃 片山, 泰佑 江野尻, 竜樹 鈴木, 茂彦 |
キーワード: | keloids fibroproliferative disorder HtrA1 inflammation |
発行日: | 24-Apr-2018 |
出版者: | MDPI AG |
誌名: | International Journal of Molecular Sciences |
巻: | 19 |
号: | 5 |
論文番号: | 1275 |
抄録: | Keloids occur after failure of the wound healing process; inflammation persists, and various treatments are ineffective. Keloid pathogenesis is still unclear. We have previously analysed the gene expression profiles in keloid tissue and found that HtrA1 was markedly up-regulated in the keloid lesions. HtrA1 is a serine protease suggested to play a role in the pathogenesis of various diseases, including age-related macular degeneration and osteoarthritis, by modulating extracellular matrix or cell surface proteins. We analysed HtrA1 localization and its role in keloid pathogenesis. Thirty keloid patients and twelve unrelated patients were enrolled for in situ hybridization, immunohistochemical, western blot, and cell proliferation analyses. Fibroblast-like cells expressed more HtrA1 in active keloid lesions than in surrounding lesions. The proportion of HtrA1-positive cells in keloids was significantly higher than that in normal skin, and HtrA1 protein was up-regulated relative to normal skin. Silencing HtrA1 gene expression significantly suppressed cell proliferation. HtrA1 was highly expressed in keloid tissues, and the suppression of the HtrA1 gene inhibited the proliferation of keloid-derived fibroblasts. HtrA1 may promote keloid development by accelerating cell proliferation and remodelling keloid-specific extracellular matrix or cell surface molecules. HtrA1 is suggested to have an important role in keloid pathogenesis. |
著作権等: | This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0). |
URI: | http://hdl.handle.net/2433/234213 |
DOI(出版社版): | 10.3390/ijms19051275 |
PubMed ID: | 29695130 |
出現コレクション: | 学術雑誌掲載論文等 |
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