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2018 ; 22
(3
): 1792-1804
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Wild-type p53 enhances endothelial barrier function by mediating RAC1 signalling
and RhoA inhibition
#MMPMID29363851
Barabutis N
; Dimitropoulou C
; Gregory B
; Catravas JD
J Cell Mol Med
2018[Mar]; 22
(3
): 1792-1804
PMID29363851
show ga
Inflammation is the major cause of endothelial barrier hyper-permeability,
associated with acute lung injury and acute respiratory distress syndrome. This
study reports that p53 "orchestrates" the defence of vascular endothelium against
LPS, by mediating the opposing actions of Rac1 and RhoA in pulmonary tissues.
Human lung microvascular endothelial cells treated with HSP90 inhibitors
activated both Rac1- and P21-activated kinase, which is an essential element of
vascular barrier function. 17AAG increased the phosphorylation of both LIMK and
cofilin, in contrast to LPS which counteracted those effects. Mouse lung
microvascular endothelial cells exposed to LPS exhibited decreased expression of
phospho-cofilin. 17AAG treatment resulted in reduced levels of active cofilin.
Silencing of cofilin pyridoxal phosphate phosphatase (PDXP) blocked the
LPS-induced hyper-permeability, and P53 inhibition reversed the 17AAG-induced
PDXP down-regulation. P190RHOGAP suppression enhanced the LPS-triggered barrier
dysfunction in endothelial monolayers. 17AAG treatment resulted in P190RHOGAP
induction and blocked the LPS-induced pMLC2 up-regulation in wild-type mice.
Pulmonary endothelial cells from "super p53" mice, which carry additional p53-tg
alleles, exhibited a lower response to LPS than the controls. Collectively, our
findings help elucidate the mechanisms by which p53 operates to enhance barrier
function.
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