Investigation of new treatment strategy for the palatal scar tissue using RLN2 carried by the target-orientated liposomes.

2023 Fiscal Year Final Research Report

• Project/Area Number: 19K22703
• Research Category: Grant-in-Aid for Challenging Research (Exploratory)
• Allocation Type: Multi-year Fund
• Review Section: Medium-sized Section 57:Oral science and related fields
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Moriyama Keiji 東京医科歯科大学, 大学院医歯学総合研究科, 教授 (20262206)
• Co-Investigator(Kenkyū-buntansha): 小川 卓也 東京医科歯科大学, 大学院医歯学総合研究科, 准教授 (50401360) ; 東堀 紀尚 東京医科歯科大学, 大学院医歯学総合研究科, 講師 (50585221) ; 小林 起穂 東京医科歯科大学, 大学院医歯学総合研究科, 助教 (20596233)
• Project Period (FY): 2019-06-28 – 2024-03-31
• Keywords: 口蓋裂 / 口蓋発生 / エピジェネティクス

Outline of Final Research Achievements

Scar tissue that develops after palatoplasty significantly affects the morphology and function of the maxillofacial-oral region in cleft palate patients throughout their lives. Currently, there is no treatment for palatal scar tissue, and this remains a challenge to overcome. We investigated the role of the histone methyltransferase SETDB1 in palatal development. We generated neural crest cell-specific Setdb1-deficient mice and examined phenotypic analysis and cell proliferative capacity in the fetal mouse palate and found that Setdb1 may affect cellular proliferative capacity and expression of Pax9, Wnt5a, and Fgf10 during palatal development. In mice with epithelial-specific deletion of Setdb1, we showed that Setdb1 may be deeply involved not only in abnormalities of the palatal epithelium but also in the process of tooth development.

Free Research Field

歯科矯正学

Academic Significance and Societal Importance of the Research Achievements

組織の瘢痕化は損傷を受けた後の創傷治癒過程で生じ、創部の閉鎖に寄与する。炎症性細胞の過剰な遊走によりTGF-βの活性化が生じ、線維芽細胞・筋線維芽細胞の増殖や活性化の結果コラーゲンなどの細胞外基質が過剰に産生されることが瘢痕組織形成の主なメカニズムとされている。得られた成果は、口蓋発生における上皮組織の増殖やメカニズムの一端を明らかとし、歯科領域にとどまらず、皮膚の瘢痕組織や臓器線維症の研究への波及効果が予想される。