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2015 Fiscal Year Final Research Report

Control of lymphocyte chemotaxis by mitochondrial metabolism

Research Project

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Project/Area Number 26670101
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field General physiology
Research InstitutionUniversity of Fukui

Principal Investigator

Matsuoka Satoshi  福井大学, 医学部, 教授 (00263096)

Project Period (FY) 2014-04-01 – 2016-03-31
Keywordsミトコンドリア / ケモタクシス / 代謝 / システム生物学
Outline of Final Research Achievements

Inhibition of mitochondrial Na+-Ca2+ exchanger (NCLX), which is strongly related with mitochondrial energy metabolism, caused attenuation of chemotaxis toward CXCL12 and augmentation of random cell movement in B lymphocytes (A20). The following mechanisms were elucidated; NCLX modulates actin polymerization and Rac1 localization through controlling cytoplasmic Ca2+ so that chemotaxis and cell motility of B lymphocytes are influenced. The control by NCLX was observed also in native B lymphocytes derived from mouse spleen, but not in T lymphocytes. It was demonstrated that the difference in Ca2+ dynamics in mitochondria and endoplasmic reticulum causes the preferential contribution of NCLX to chemotaxis in B lymphocytes. In addition, it was suggested that mitochondrial beta-oxidation has important roles in cell motility and chemotaxis of B lymphocytes.

Free Research Field

細胞生理学

URL: 

Published: 2017-05-10  

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