The mechanism of microRNA in inflammatory bowel disease model mouse

• Project/Area Number: 18K07078
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 49030:Experimental pathology-related
• Research Institution: Kansai Medical University
• Principal Investigator: ANDO YUGO 関西医科大学, 医学部, 講師 (50388427)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Project Status: Completed (Fiscal Year 2020)
• Budget Amount: ¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000); Fiscal Year 2020: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000); Fiscal Year 2019: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000); Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
• Keywords: miR-21 / microRNA / IBD / UC / CD / PDCD4 / 炎症性腸疾患

Outline of Final Research Achievements

It has been reported that miR-21 is highly expressed in the intestinal mucosa of patients with inflammatory bowel disease (IBD) and IBD model mice. It has not been clarified the mechanism of miR-21 in the onset and chronicity of enteritis. In this study, we examined the role of miR-21 in vivo using dominant negative TGF-β Receptor II mice, which is one of IBD model mice.
Knockout of miR-21 exacerbated enteritis in the IBD model mice, suggesting that miR-21 may play a critical role to suppress the local inflammation of the colon.

Academic Significance and Societal Importance of the Research Achievements

現在、難病である潰瘍性大腸炎やクローン病などの炎症性腸疾患（IBD)の患者数は年々増加傾向にあります。しかもIBDは若年発症する患者が大多数を占めており、難治例では患者の人生設計に大きな影響を与える可能性があります。また、難治性症例では生物学的製剤などの高額な医療費が継続的に必要となり、医療経済的にも大きな負担となっています。現在、まだIBDの根本原因は同定されていないため、根治治療法は確立されておらず、寛解維持が治療のゴールと考えられています。今回の我々が行なった基礎的な研究成果が、近い将来、疾患の原因究明や疾患活動性マーカー、新規薬剤の開発に寄与する可能性が考えらる。