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Angiotensin II stimulates the synthesis of vascular endothelial growth factor through the p38 mitogen activated protein kinase pathway in cultured mouse podocytesopen access

Authors
Kang, YSPark, YGKim, BKHan, SYJee, YHHan, KHLee, MHSong, HKCha, DRKang, SWHan, DS
Issue Date
Apr-2006
Publisher
BIOSCIENTIFICA LTD
Citation
JOURNAL OF MOLECULAR ENDOCRINOLOGY, v.36, no.2, pp.377 - 388
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF MOLECULAR ENDOCRINOLOGY
Volume
36
Number
2
Start Page
377
End Page
388
URI
https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/18918
DOI
10.1677/jme.1.02033
ISSN
0952-5041
Abstract
Angiotensin II (Ang-II) and vascular endothelial growth factor (VEGF) have an important role in the pathogenesis of diabetic nephropathy, but the signaling cascade of VEGF regulation in response to Ang-II in podocytes is largely unknown. In these experiments, we looked at the effect of Ang-II on the production of VEGF, and investigated whether VEGF production depends on the p38 mitogen activated protein kinase (MAPK) pathway in cultured mouse podocytes. Incubation of podocytes with Ang-II induced a rapid increase in VEGF mRNA expression and protein synthesis as well as its transcriptional activity in an Ang-II dose-dependent manner. To further define the role of angiotensin type 1 (AT1) and type 2 (AT2) receptors involved in Ang-II-mediated VEGF synthesis, the effects of selective AT1 and AT2 receptor antagonists were evaluated. Prior treatment with losartan significantly inhibited VEGF mRNA and protein synthesis induced by Ang-II, which suggests that the AT1 receptor is involved in Ang-II-mediated VEGF synthesis. Furthermore, stimulation of the cells with Ang-II increased both phosphorylation of p38 MAPK and MAP kinase kinase 3/6 (MKK3/6). Additionally, Ang-II enhanced the DNA binding activity to CAMP response element binding protein (CREB) and phosphorylation of CREB. In addition, to investigate the role of p38 MAPK in Ang-II-incluced VEGF synthesis, podocytes were pretreated with or without the p38 MAPK inhibitor, SB203580 for 24 h to observe whether Ang-II-mediated VEGF synthesis was inhibited by blocking p38 MAPK The addition of SB203580 led to a marked inhibition of the increased VEGF mRNA and protein production induced by Ang-II in a dose-dependent manner. Taken together, these results suggest that Ang-II stimulates the synthesis of VEGF in podocytes and the production of VEGF induced by Ang-II is mediated, in part, through the activation of the p38 MAPK pathway.
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1. Basic Science > Department of Biochemistry and Molecular Biology > 1. Journal Articles
2. Clinical Science > Department of Nephrology and Hypertension > 1. Journal Articles

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College of Medicine (Department of Biochemistry and Molecular Biology)
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