| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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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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