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Study of the mechanism of tubuloglomerular feedback in macula densa

Research Project

Project/Area Number 12671053
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Kidney internal medicine
Research InstitutionSaitama Medical School (2002)
Jikei University School of Medicine (2000-2001)

Principal Investigator

HASEGAWA Hajime  SAITAMA MEDICAL SCHOOL, ASSISTANT PROFESSOR, 医学部, 講師 (30231517)

Project Period (FY) 2000 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
Keywordstubuloglomerular feedback / Na-K-2Cl cotransporter / aquaporin / renal failure / DM nephropathy / Na-Cl共輸送体 / tubuloglomerular feedback / マクラデンサ / tubulo-glomerular feedback
Research Abstract

In this study, the involvement of tubuloglomerular feedback (TGF) abnormality was studied. First, macula densa specific NKCC homolog was identified based on homology cloning strategy. Second, its expression was principally studied by in situ PCR hybridization method. Subsequently, the changes of its gene expression in urinary tract obstruction (UTO) model and non-insulin dependent diabetes mellitus model (NIDDM) were studied. As a results, expression of new clone was decreased in NIDDM, suggesting that its abolished expression might generate the suppression of TGF and expose high pressure to glomerulus, causing glomerulosclerosis.

Report

(4 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • 2000 Annual Research Report

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Published: 2000-04-01   Modified: 2016-04-21  

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