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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 J+Cell+Mol+Med
2015 ; 19
(6
): 1400-9
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Renalase contributes to the renal protection of delayed ischaemic preconditioning
via the regulation of hypoxia-inducible factor-1?
#MMPMID25781495
Wang F
; Zhang G
; Xing T
; Lu Z
; Li J
; Peng C
; Liu G
; Wang N
J Cell Mol Med
2015[Jun]; 19
(6
): 1400-9
PMID25781495
show ga
Ischaemic preconditioning (IPC) attenuates acute kidney injury (AKI) from renal
ischaemia reperfusion. Renalase, an amine oxidase secreted by the proximal
tubule, not only degrades circulating catecholamines but also protects against
renal ischaemia reperfusion injury. Here, it has been suggested that the
renoprotective effect of renal IPC is partly mediated by renalase. In a model of
brief intermittent renal IPC, the increased cortex renalase expression was found
to last for 48 hrs. IPC significantly reduced renal tubular inflammation,
necrosis and oxidative stress following renal ischaemia reperfusion injury. Such
effects were attenuated by blocking renalase with an anti-renalase monoclonal
antibody. We further demonstrated that renalase expression was up-regulated by
hypoxia in vitro via an hypoxia-inducible factor (HIF)-1? mechanism. The
IPC-induced up-regulation of renalase in vivo was also reduced by pre-treatment
with an HIF-1? inhibitor, 3-(5'-Hydroxymethyl-2'-furyl)-1-benzyl indazole. In
summary, the renoprotective effect of IPC is partly dependent on the renalase
expression, which may be triggered by hypoxia via an HIF-1? mechanism. Endogenous
renalase shows potential as a therapeutic agent for the prevention and treatment
of AKI.