Hypoxia-induced expression of phosducin-like 3 regulates expression of VEGFR-2 and promotes angiogenesis

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Hypoxia-induced expression of phosducin-like 3 regulates expression of VEGFR-2 and promotes angiogenesis

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Title: Hypoxia-induced expression of phosducin-like 3 regulates expression of VEGFR-2 and promotes angiogenesis
Author: Srinivasan, Srimathi; Chitalia, Vipul; Meyer, Rosana D.; Hartsough, Edward; Mehta, Manisha; Harrold, Itrat; Anderson, Nicole; Feng, Hui; Smith, Lois Elaine Hodgson; Jiang, Yan; Costello, Catherine E.; Rahimi, Nader

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Citation: Srinivasan, Srimathi, Vipul Chitalia, Rosana D. Meyer, Edward Hartsough, Manisha Mehta, Itrat Harrold, Nicole Anderson, et al. 2015. Hypoxia-Induced Expression of Phosducin-Like 3 Regulates Expression of VEGFR-2 and Promotes Angiogenesis. Angiogenesis 18, no. 4: 449–462. doi:10.1007/s10456-015-9468-3.
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Abstract: Expression and activation of vascular endothelial growth factor receptor 2 (VEGFR-2) by VEGF ligands are the main events in the stimulation of pathological angiogenesis. VEGFR-2 expression is generally low in the healthy adult blood vessels, but its expression is markedly increased in the pathological angiogenesis. In this report, we demonstrate that phosducin-like 3 (PDCL3), a recently identified chaperone protein involved in the regulation of VEGFR-2 expression, is required for angiogenesis in zebrafish and mouse. PDCL3 undergoes N-terminal methionine acetylation, and this modification affects PDCL3 expression and its interaction with VEGFR-2. Expression of PDCL3 is regulated by hypoxia, the known stimulator of angiogenesis. The mutant PDCL3 that is unable to undergo N-terminal methionine acetylation was refractory to the effect of hypoxia. The siRNA-mediated silencing of PDCL3 decreased VEGFR-2 expression resulting in a decrease in VEGF-induced VEGFR-2 phosphorylation, whereas PDCL3 over-expression increased VEGFR-2 protein. Furthermore, we show that PDCL3 protects VEGFR-2 from misfolding and aggregation. The data provide new insights for the chaperone function of PDCL3 in angiogenesis and the roles of hypoxia and N-terminal methionine acetylation in PDCL3 expression and its effect on VEGFR-2.
Published Version: doi:10.1007/s10456-015-9468-3
Other Sources: http://www.ncbi.nlm.nih.gov/pubmed/26059764
Terms of Use: This article is made available under the terms and conditions applicable to Open Access Policy Articles, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#OAP
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:33776185
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