Analysis of Regulatory Mechanism of RANK Gene Expression

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08426
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Ehime University
• Principal Investigator: KITAZWA RIKO 愛媛大学, 医学部附属病院, 准教授 (00273780)
• Co-Investigator(Kenkyū-buntansha): 原口 竜摩 愛媛大学, 医学系研究科, 講師 (00423690) ; 水野 洋輔 愛媛大学, 医学部附属病院, 助教 (90748021)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 破骨細胞 / RANK / 遺伝子プロモータ / 遺伝子改変動物

Outline of Final Research Achievements

Receptor activator of NF-kB (RANK) is a member of the TNF receptor family expressed in osteoclast precursors, and RANK-RANK ligand signaling is essential for osteoclastogenesis. We have identified a novel alternative splicing variant of RANK gene (vRANK) encoding the short molecule. When overexpressed in vitro, vRANK in RAW264.7 cells decreased the formation of osteoclasts. When systemically overexpressed in vivo, the CAGcre+/vRANK mouse showed high fatality. When selectively overexpressed among the monocyte-macrophage lineage, the LysMcre+/vRANK mouse showed decreased osteoclastogenesis in ex vivo culture of spleen cells, and increased bone mass measured by micro CT. These results suggest that vRANK is a novel bioactive peptide that might educes the number of osteoclasts

Free Research Field

病理学