Mechanistic analysis of onset and progress of periodontitis causing microRNA

2015 Fiscal Year Final Research Report

• Project/Area Number: 25463229
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Periodontology
• Research Institution: Nihon University
• Principal Investigator: OGATA Yorimasa 日本大学, 松戸歯学部, 教授 (90204065)
• Co-Investigator(Kenkyū-buntansha): NAKAYAMA Yohei 日本大学, 松戸歯学部, 専任講師 (30434088) ; TAKAI Hideki 日本大学, 松戸歯学部, 専任講師 (30453898)
• Research Collaborator: MATSUMURA Hiroyoshi ; MATSUI Sari ; KATO Ayako
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: microRNA / サイトカイン / 遺伝子発現 / タンパク質発現 / 歯肉線維芽細胞 / 炎症 / 歯周炎

Outline of Final Research Achievements

MicroRNAs (miRNAs) can bind to target mRNAs through partial complementarity and regulate many genes. To determine the effects of miR-223 on the expressions of IL-1β and IL-6, HGF were stimulated by IL-1β (1 ng/mL) or TNFα (10 ng/mL) and transfected with a miR-223 expression plasmid. Levels of mRNA for IL-1β, IL-6, inhibitor of kappa-B kinase α (IKKα) and mitogen-activated protein kinase phosphatase-5 (MKP-5) were measured by real-time PCR, and levels IL-1β, IL-6 and IKKα protein were determined by enzyme-linked immunosorbent assay and Western blotting. Expression of IL-1β and IL-6 mRNAs was induced by IL-1β and TNFα and further increased by miR-223 overexpression. IL-1β and TNFα induced the expression of IL-1β and IL-6 mRNAs, and this was reduced by miR-223 inhibitor. Overexpression of miR-223 decreased the levels of IKKα protein and MKP-5 mRNA in HGF. These findings indicate that miR-223 might control the inflammatory response via IKKα and MKP-5 in periodontal tissue.

Free Research Field

歯周病学