期刊
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
卷 10, 期 1, 页码 25-35出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.niox.2004.02.001
关键词
nitric oxide; IGF-1; VEGF; rat glomeruli; endothelial nitric oxide synthase; expression; phosphorylation; phosphatidylinositol 3-kinase
Nitric oxide (NO) is reported to be involved in the pathogenesis of renal hyperfiltration in the early stage of diabetic nephropathy. We set out to determine whether IGF-I and/or VEGF(165) directly stimulate NO production in rat glomeruli and whether the expression of NO synthase (NOS) isoforms as well as eNOS phosphorylation contribute to NO generation by IGF-I and VEGF. Long-term exposure to IGF-I and/or VEGF165 augments NO production through increased eNOS mRNA, protein expression and phosphatidylinositol 3-kinase (P13-K) signaling pathway plays a major role in this process; short-term exposure to IGF-I and/or VEGF165 activates eNOS activity via phosphorylation by a P13-K/Akt dependent pathway. Our data suggest the great possibility that increased endogenous IGF-I and VEGF may be responsible for the up-regulation of eNOS expression and NO production which contributes to glomerular hyperfiltration in early diabetic kidneys. IGF-I is a newly described growth factor that up-regulates eNOS expression and P13-K plays a major role in this process. (C) 2004 Elsevier Inc. All rights reserved.
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