Regulation of pericellular proteolysis and neural development

2014 Fiscal Year Final Research Report

• Project Area: Neural Diversity and Neocortical Organization
• Project/Area Number: 22123005
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Kyoto University
• Principal Investigator: NODA Makoto 京都大学, 医学(系)研究科(研究院), 教授 (30146708)
• Co-Investigator(Renkei-kenkyūsha): MATSUZAKI Tomoko 京都大学, 医学研究科, 助教 (50402855) ; IMAMURA Yukio 京都大学, 医学研究科, 助教 (90447954)
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: 組織細胞 / 神経科学 / 生体分子 / 脳・神経 / 発生・分化

Outline of Final Research Achievements

We investigated the effects of RECK on brain development and cellular behaviors in multiple experimental systems in vivo and in vitro. In vivo, we found that selective inactivation of Reck in vascular endothelial cells in mice results in perinatal death with severe disruption of tissue structure in the cerebral neocortex. Mice with selective inactivation of Reck in neural precursor cells, on the other hand, were found to be viable and show no obvious phenotypes. Close investigations, however, revealed that these mice had altered neocortical cytoarchitecture and show interesting behavioral phenotypes, such as anxiety-like and perseverative behaviors and reduced pre-pulse inhibition. In vitro, RECK was found to suppress cell cycle progression by downregulating SKP2, to be induced after epithelial-mesenchymal transition in normal cells but not in cancer cells, and to suppress fibrosis by inhibiting migration of cardiac fibroblasts.

Free Research Field

分子腫瘍学