2015 Fiscal Year Final Research Report
Control of lymphocyte chemotaxis by mitochondrial metabolism
| Project/Area Number |
26670101
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | University of Fukui |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Keywords | ミトコンドリア / ケモタクシス / 代謝 / システム生物学 |
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| 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.
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| Free Research Field |
細胞生理学
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