Study of the association between adipocytes and fibroblasts for keloid pathogenesis

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K09474
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 56070:Plastic and reconstructive surgery-related
• Research Institution: Tohoku University
• Principal Investigator: Nagao Munetomo 東北大学, 大学病院, 助教 (00364349)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: ケロイド / 肥厚性瘢痕 / 創傷治癒 / 線維芽細胞 / 脂肪細胞 / ケモカイン

Outline of Final Research Achievements

It has been known that undifferentiated fibroblasts are called preadipocytes (Alessi MC.et.al. Horm Metab Res, 2000 et al.). In other words, we hypothesized that progenitor cells, which would normally be replaced by adipocytes, would transform into abnormal fibroblasts, leading to a spiral of fibrotic proliferation, which would result in keloids and hypertrophic scars.
We focused on chemokines, which play an important role in the mobilization of progenitor cells and other cells, and conducted a chemokine-targeted analysis using a mouse model of hypertrophic scars. The results suggest the possibility of a new treatment for hypertrophic scars.

Free Research Field

ケロイド、創傷治癒、血管腫、脈管奇形

Academic Significance and Societal Importance of the Research Achievements

いわゆる真性ケロイドは多発性に醜状瘢痕、疼痛、掻痒を伴い、患者は長期的に通院を余儀なくされ、著しくQOLが落ちる。そのため、ケロイドの機序解明、新たな治療法の開発は、そのような患者にとっても切実な願いである。
本研究においては、ケロイドや肥厚性瘢痕の発生過程における線維芽細胞と脂肪細胞の関連性につき、その細胞動員に重要な役割を担っているケモカインに着目して、研究を進めた。肥厚性瘢痕モデルマウスを用いて解析を行ない、新たな肥厚性瘢痕治療の可能性が見出された。