| Project/Area Number |
15H06038
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tohoku University |
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Principal Investigator |
Narumi Kaori 東北大学, 大学病院, 助教 (40754130)
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| Research Collaborator |
Sato Emiko 東北大学, 薬学系研究科, 助教 (20466543)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | プロレニンレセプター / メサンギウム細胞 / インドキシル硫酸 / 慢性腎臓病 / 内科 / (プロ)レニンレセプター |
|---|
| Outline of Final Research Achievements |
We collected sera from patients diagnosed with immunoglobulin A nephropathy by renal biopsy and examined the correlation between serum soluble (P)RR [s(P)RR] and various laboratory data and pathological indices. The s(P)RR level significantly correlated with the level of mesangial expansion and serum indoxyl sulfate (IS). To investigate the association between (P)RR and mesangial fibrosis or expansion, we used mouse mesangial cell line SV40 MES13. (P)RR expression significantly increased in the presence of IS. IS stimulation enhanced the expression of the fibrotic factors, this increased expression was significantly suppressed by knockdown of (P)RR. Moreover, it significantly increased the expression of tissue inhibitor of metalloproteinase type 1 and matrix metalloproteinase 9 via the ERK1/2 pathway in SV40 MES13 cells. Our results suggest that in the presence of IS, (P)RR is associated with mesangial fibrosis and matrix expansion through the (P)RR-mediated ERK1/2 pathway.
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