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Title 

Regulation of PDGF signalling and vascular remodelling by peroxiredoxin II

Authors 

M H ChoiI K LeeG W KimB U KimYing Hao HanDae Yeul YuH S ParkK Y KimJ S LeeC ChoiY S BaeB I LeeS G RheeS W Kang

Publisher 

Nature Publishing Group

Issue Date 

2005

Citation 

Nature, vol. 435, no. 7040, pp. 347-353

Keywords 

platelet-derived growth factor (PDGF)vascular remodelingcardiovascular systemperoxiredoxincardiovascular diseasevascular smooth muscleneovascularization, physiologic

Abstract 

Platelet-derived growth factor (PDGF) is a potent mitogenic and migratory factor that regulates the tyrosine phosphorylation of a variety of signalling proteins via intracellular production of H2O2 (refs 1-3). Mammalian 2-Cys peroxiredoxin type II (Prx II; gene symbol Prdx2) is a cellular peroxidase that eliminates endogenous H2O2 produced in response to growth factors such as PDGF and epidermal growth factor; however, its involvement in growth factor signalling is largely unknown. Here we show that Prx II is a negative regulator of PDGF signalling. Prx II deficiency results in increased production of H2O2, enhanced activation of PDGF receptor (PDGFR) and phospholipase Cγ1, and subsequently increased cell proliferation and migration in response to PDGF. These responses are suppressed by expression of wild-type Prx II, but not an inactive mutant. Notably, Prx II is recruited to PDGFR upon PDGF stimulation, and suppresses protein tyrosine phosphatase inactivation. Prx II also leads to the suppression of PDGFR activation in primary culture and a murine restenosis model, including PDGF-dependent neointimal thickening of vascular smooth muscle cells. These results demonstrate a localized role for endogenous H 2O2 in PDGF signalling, and indicate a biological function of Prx II in cardiovascular disease.

ISSN 

0028-0836

Link 

http://dx.doi.org/10.1038/nature03587

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2017-04-19


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