Research on pathophysiology toward a treatment method for painful scars by regenerating the skeletal muscle system

2022 Fiscal Year Final Research Report

• Project/Area Number: 19K07853
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 51030:Pathophysiologic neuroscience-related
• Research Institution: Aichi Medical University
• Principal Investigator: Ushida Takahiro 愛知医科大学, 医学部, 教授 (60304680)
• Co-Investigator(Kenkyū-buntansha): 木全 弘治 愛知医科大学, 災害医療研究センター, 名誉教授 (10022641) ; 太田 明伸 愛知医科大学, 医学部, 講師 (30438048)
• Project Period (FY): 2019-04-01 – 2023-03-31
• Keywords: 慢性疼痛 / 瘢痕性疼痛 / 遺伝子解析 / ノイロトロピン

Outline of Final Research Achievements

n this study, two animal models were created to evaluate the effects of treatment of tissue damage. In model 1), a mouse model of plantar cicatricial pain was used, and a decrease in mechanical threshold and swelling were observed. Observed decreased swelling and improved pain threshold after topical administration of an inflammatory skin extract (NTP) from vaccinia virus-inoculated house rabbits. In model 2), a tibialis anterior muscle avulsion model was used and similar results were obtained with topical administration of NTP. In our analysis, we used model 1) to explore molecular mechanisms related to tissue regeneration, and analyzed gene expression using RT-PCR and microarray methods, suggesting that cascades such as ECM-receptor interaction are suppressed by NTP treatment, which may be involved in scarring and pain exacerbation.

Free Research Field

慢性疼痛

Academic Significance and Societal Importance of the Research Achievements

瘢痕性疼痛モデル動物を用いて筋肉および周囲組織の再生に関わる細胞外環境と反応の分子機序の解明を目指した。DRGではTGF-beta signaling pathway、ECM-receptor interaction（以下ERI）とNeurotrophin signaling pathwayは瘢痕手術後に活性化されたが、NTP治療後に抑制された。また、足底瘢痕組織ではERIとCytokine-cytokine receptor interactionが活性化され、 ERIがNTP治療で抑制が見られた。NTP治療で抑制されたカスケードが瘢痕やそれによる痛みの増悪への関与が推察された。