2015 Fiscal Year Final Research Report
MafB regulate C1q genes in macrophage
| Project/Area Number |
25860205
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | マクロファージ / MafB / C1q |
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| Outline of Final Research Achievements |
Transcription factor MafB is specifically expressed in macrophages in hematopoietic cells. During the adult stage, both Mafb-deficient fetal liver cells that were transplanted into recipient mice and macrophage-specific Mafb conditional knock-out mice exhibited autoimmune phenotypes. Macrophage efferocytosis (apoptotic cells uptake) is important for inhibiting autoimmune disease. The efferocytosis ability of Mafb-deficient macrophages was strongly reduced. The expression of complement component-1q (C1q), which is known as the first protein in the classical complement pathway and for mediating efferocytosis, was reduced in Mafb-null macrophages. The promoter analysis of C1q genes showed that MafB directly regulates C1qa, C1qb, and C1qc promoter. Consistent with this result, the classical pathway was also decreased in Mafb-deficient mice analyzed by hemolysis assay. These results suggest that MafB primarily regulates C1q genes.
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| Free Research Field |
分子生物学
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