Activation mechanism of the cellular Factor XIII for nerve regeneration

2017 Fiscal Year Final Research Report

• Project/Area Number: 26350958
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Biomolecular chemistry
• Research Institution: Kanazawa University
• Principal Investigator: SUGITANI Kayo 金沢大学, 保健学系, 助教 (20162258)
• Co-Investigator(Kenkyū-buntansha): 北村 敬一郎 金沢大学, 保健学系, 教授 (80283117) ; 郡山 恵樹 鈴鹿医療科学大学, 薬学部, 准教授 (70397199)
• Research Collaborator: NODA Masaharu 基礎生物学研究所, 教授 (60172798) ; SHINTANI Takafumi 基礎生物学研究所, 准教授 (10312208) ; KATO Satoru 金沢大学, 健康増進科学センター, 研究協力員 (10019614) ; HITOMI Kiyotaka 名古屋大学, 大学院創薬科学研究科, 教授 (00202276)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: Factor XIII-A / CNS regeneration / optic nerve / retina / cellular Factor XIII / zebrafish / activation peptide / repair

Outline of Final Research Achievements

Factor XIII-A (FXIII-A), also known as cellular transglutaminase, plays important roles in mediating cross-linking reactions in various tissues. Previous research has shown that FXIII-A was immediately upregulated in the fish retina and optic nerve after nerve injury. However, the activation mechanism of the FXIII-A remains unclear. Here, we investigated the activation mechanism of the FXIII-A using zebrafish CNS regeneration system. Thrombin mRNA was undetectable in zebrafish optic nerve and retina both before and after optic nerve injury. Sequence analysis of FXIII-A 5'-RACE products showed that most of clones derived from intact retina showed full sequence of FXIII-A, however, many clones derived from injured retina showed short sequences of FXIII-A which lacked exon 1-2 region. Therefore, unlike plasma FXIII-A, activation of FXIII-A in injured retina and optic nerve does not need the cleavage by thrombin, may occur the directly production of activated FXIII-A protein.

Free Research Field

神経化学，分子生物学、臨床検査学