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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Angiogenesis
2015 ; 18
(4
): 449-62
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Hypoxia-induced expression of phosducin-like 3 regulates expression of VEGFR-2
and promotes angiogenesis
#MMPMID26059764
Srinivasan S
; Chitalia V
; Meyer RD
; Hartsough E
; Mehta M
; Harrold I
; Anderson N
; Feng H
; Smith LE
; Jiang Y
; Costello CE
; Rahimi N
Angiogenesis
2015[Oct]; 18
(4
): 449-62
PMID26059764
show ga
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.
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