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Open AccessArticle

HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloid Development

1
Department of Plastic and Reconstructive Surgery, Japanese Red Cross Fukui Hospital, 2-4-1, Tsukimi, Fukui-City, Fukui 918-8501, Japan
2
Department of Plastic and Reconstructive Surgery, Graduate School of Medicine, Kyoto University, 54 Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
3
Department of Life Science, Faculty of Engineering Science, Akita University, 1-1 Tegata Gakuenmachi, Akita 010-8502, Japan
4
Department of Plastic and Reconstructive Surgery, Japanese Red Cross Otsu Hospital, 1-1-35, Nagara, Otsu City, Shiga 520-8511, Japan
5
Department of Plastic and Reconstructive Surgery, Shiga Medical Center for Adults, 5-4-30, Moriyama, Moriyama City, Shiga 524-8524, Japan
6
Department of Plastic and Reconstructive Surgery, Kobe City Medical Center General Hospital, 2-1-1, Minatojima minami-machi, Cyuou-ku, Kobe City, Hyogo 650-0047, Japan
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2018, 19(5), 1275; https://doi.org/10.3390/ijms19051275
Received: 3 March 2018 / Revised: 4 April 2018 / Accepted: 16 April 2018 / Published: 24 April 2018
(This article belongs to the Special Issue Recent Advances in Scar Biology)
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. View Full-Text
Keywords: keloids; fibroproliferative disorder; HtrA1; inflammation keloids; fibroproliferative disorder; HtrA1; inflammation
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Yamawaki, S.; Naitoh, M.; Kubota, H.; Aya, R.; Katayama, Y.; Ishiko, T.; Tamura, T.; Yoshikawa, K.; Enoshiri, T.; Ikeda, M.; Suzuki, S. HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloid Development. Int. J. Mol. Sci. 2018, 19, 1275.

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