1996 Fiscal Year Final Research Report Summary
Defense mechanism of glomerular visceral epithelial cells against stress
Project/Area Number |
07807105
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | Niigata University |
Principal Investigator |
YAOITA Eishin School of Medicine, Niigata University Assistant, 医学部, 助手 (00157950)
|
Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Tadashi School of Medicine, Niigata University Associate Prof., 医学部, 助教授 (30092737)
|
Project Period (FY) |
1995 – 1996
|
Keywords | glomerulus / visceral epithelial cells / intermediate filament / desmin / vimentin / plectin |
Research Abstract |
Glomerular visceral epithelial cells (VECs) in mammals contain abundant intermediate filaments (IFs) in comparison with tubular epithelial cells. An extensive investigation of various species from amphibia to mammals showed that the characteristic was common to lower vertebrate, suggesting an important role of IF in VECs. Rat VECs express desmin. In Masugi nephritis, the staining intensity of desmin was parallel with the amount of injected dose of anti-GBM antisera and proteinuria. In puromycin aminonucleoside nephrosis, increase and decrease of the amount of desmin in VECs was shown to be parallel to proteinuria by Western blotting and immunostaining. These findings indicated that desmin expression in VECs was influenced by the condition under stress such as nephrosis. Plectin is an IF-associated protein which is postulated to function as a general cytoplasmic cross-linking element of IFs. Depending on cell types, plectin was found primarily either through the cytoplasm, at the cell periphery, or in the both location. VECs uniquely showed plectin attached predominantly to the perinuclear region. The cytoplasmic staining became intense in puromycine aminonucleoside nephrosis. We hypothesize that abundant IFs and uniquely distributed plectin in VECs function to resist mechanical stress produced by ultrafiltrate from slit diaphragm and pulsing capillary walls.
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[Publications] S.Goto, T.Yamamoto, Lili Feng, E.Yaoita, S.Hirose, H.Fujinaka, K.Kawasaki, R.Hattori, Y.Yui, C.B.Wilson, M.Arakawa, I.Kihara: "Expression and localization of inducible nitric oxide synthase in anti-Thy-1 glomerulonephritis." Am.J.Pathol.147. 1133-1141 (1995)
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