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2014 Fiscal Year Final Research Report

Elucidation of pathogenesis and progression mechanisms of glomerulonephritis through prostaglandin E2-renal dendritic cell axis

Research Project

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Project/Area Number 25860692
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Kidney internal medicine
Research InstitutionNippon Medical School

Principal Investigator

NAGASAKA Shinya  日本医科大学, 医学部, 助教 (00573239)

Project Period (FY) 2013-04-01 – 2015-03-31
Keywords腎局在樹状細胞 / プロスタグランジンE2 (PGE2) / 腎疾患
Outline of Final Research Achievements

I showed the novel phenotype of renal dendritic cell (RDC), CD11c+F4/80+PDCA1+. Furthermore, RDCs expressed PGE2 receptor as well as Cox-2 and mPGES-1 molecule involved in prostaglandin E2 synthesis which is known as an inflammatory mediator. These findings suggested that RDC function might be regulated by PGE2 autocrine manner.
In in vivo experiment, the population of RDCs in UUO (unilateral ureteral obstruction) mouse kidney were decreased, in which model is known that PGE2 expression is upregulated. However, the expressions of MHC classII molecule, IL-12/23p40 and IL-23p19 were significantly increased in RDCs migrated in UUO kidney.

Free Research Field

腎臓学、免疫学、分子生物学、細胞生物学

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Published: 2016-06-03  

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