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고포도당이 백서 사구체 메산지움 세포의 Nitric Oxide 합성에 미치는 영향

Other Titles
 Effect of High Glucose on Nitric Oxide Production in Culteured Rat Mesangial Cells 
Authors
 노현진  ;  하헌주  ;  유미라  ;  신석균  ;  송현용  ;  황재하  ;  강신욱  ;  최규헌  ;  한대석  ;  이호영 
Citation
 Korean Journal of Nephrology (대한신장학회지), Vol.18(6) : 856-868, 1999 
Journal Title
Korean Journal of Nephrology(대한신장학회지)
ISSN
 1225-0015 
Issue Date
1999
Abstract
Diabetic nephopathy is one of the leading causes of end-stage renal disease and characterized pathologically by the glomerular mesangial expansion and increased extracellular matrix(ECM) formation. Glomerular hyper-filtration and increased vascular permeability observed in the early stage of diabetic nephropathy have been proposed to play a significant pathophysiologic role in the eventual development of glomerulosclerosis of dia-betic nephropathy. Some studies have suggested that this glomerular hyperfiltration is mediated by increased nitric oxide(NO) production via the constitutive nitric oxide synthase(cNOS) pathway present in endothelial cells under the high glucose environment. However, the exact role of the inducible NOS(iNOS) pathway present in mesangial cells in the pathogenesis of diabetic neph-ropathy is not clearly established. The present study was carried out to examine whether NO production via the iNOS pathway is mo-dulated in cultured rat mesangial cells exposed to the high glucose environment and underlying mechanism of this modulation. For this purpose, the production of the stable metabolite of NO(nitrite), intracellular cyclic gu-anosine monophosphate(cGMP), iNOS mRNA expression and iNOS protein synthesis were examined under different glucose concentrations. Rat mesangial cells cultured in high glucose concen- tration(30mM D-glucose) increased significantly nitrit#e/ nitrate production and intracellular cGMP levels upon stimulation with lipopolysaccharide(LPS) plus interfer-on-r (IFN-r ) compared with control glucose concen- tration(5.6mM D-glucose). Mesangial iNOS mRNA expression and protein synthesis also increased signifi- cantly in response to high glucose. This enhanced iNOS mRNA expression induced by high glucose concentration was significantly suppressed by protein kinase C(PKC) inhibitor, calphostin C, and the aldose
reductase inhibitor, 6-bromo-l, 3-dioxo-1H- benz[d, elisoquinoline-2(3H)-acetic acid. These results indicate that high glucose in combination with stimulation by LPS plus IFN- r enhances NO production from mesangial cells by the iNOS pathway, and that the activation of PKC and the polyol pathway may play a role in this enhancement.
Files in This Item:
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Shin Wook(강신욱) ORCID logo https://orcid.org/0000-0002-5677-4756
Choi, Kyu Hun(최규헌) ORCID logo https://orcid.org/0000-0003-0095-9011
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/174056
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