| Project/Area Number |
12671021
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | GUNMA UNIVERSITY |
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Principal Investigator |
NOJIMA Yosihisa GUNMA UNIVERSITY THIRD DEPARTMENT OF INTERNAL MEDICINE PROFESSOR, 医学部, 教授 (90201699)
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| Co-Investigator(Kenkyū-buntansha) |
UEKI Kazue GUNMA UMVERSITY THIRD DEPARTMENT OF INTERNAL MEDICINE INSTRUCTOR, 医学部, 助手 (20272239)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2001: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | crescentic glomerulonephritis / tyrosine kinase |
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| Research Abstract |
Cell adhesion kinase b (CAKβ, also known as Pyk2/CadTK/RAFTK) is the second member of the focal adhesion kinase (FAK) subfamily. In the current study, we examined the expression of CAKβ in various human glomerulopathies by immunohistochemistry. While CAKβ expression in the normal kidney is confined to the brush border of the proximal tubule with no detectable glomerular staining, we found that glomerular crescents strongly expressed this kinase. Expression of CAKβ was prominent in cellular crescents, but was minimal in fibrocellular or fibrous crescents. Serial section analysis revealed that a majority of CAKβ-expressing cells were positive for cytokeratin but were negative for CD68 (a macrophage marker), suggesting that CAKβ was expressed by parietal epithelium in the crescents. We also examined CAKβ expression in a rat model of crescentic glomerulonephritis (CrGN) induced by anti-glomerular basement membrane antibody. Like human nephritis, enhanced expression of CAKβ in glomerular crescents was apparent. Increased expression of CAKb was also confirmed by anti-CAKb immunoblotting as well as by real-time quantitative PCR. Previous studies have shown that CAKβ is activated by various stimuli regulating cell growth and survival. Although our findings do not determine whether or not increased expression of CAKβ is a primary event for the development of CrGN, further understanding of this pathway may be important to gain novel insights into the factors that promote crescent formation.
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