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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 Am+J+Physiol+Renal+Physiol
2015 ; 308
(12
): F1452-62
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Muc1 is protective during kidney ischemia-reperfusion injury
#MMPMID25925251
Pastor-Soler NM
; Sutton TA
; Mang HE
; Kinlough CL
; Gendler SJ
; Madsen CS
; Bastacky SI
; Ho J
; Al-Bataineh MM
; Hallows KR
; Singh S
; Monga SP
; Kobayashi H
; Haase VH
; Hughey RP
Am J Physiol Renal Physiol
2015[Jun]; 308
(12
): F1452-62
PMID25925251
show ga
Ischemia-reperfusion injury (IRI) due to hypotension is a common cause of human
acute kidney injury (AKI). Hypoxia-inducible transcription factors (HIFs)
orchestrate a protective response in renal endothelial and epithelial cells in
AKI models. As human mucin 1 (MUC1) is induced by hypoxia and enhances HIF-1
activity in cultured epithelial cells, we asked whether mouse mucin 1 (Muc1)
regulates HIF-1 activity in kidney tissue during IRI. Whereas Muc1 was localized
on the apical surface of the thick ascending limb, distal convoluted tubule, and
collecting duct in the kidneys of sham-treated mice, Muc1 appeared in the
cytoplasm and nucleus of all tubular epithelia during IRI. Muc1 was induced
during IRI, and Muc1 transcripts and protein were also present in recovering
proximal tubule cells. Kidney damage was worse and recovery was blocked during
IRI in Muc1 knockout mice compared with congenic control mice. Muc1 knockout mice
had reduced levels of HIF-1?, reduced or aberrant induction of HIF-1 target genes
involved in the shift of glucose metabolism to glycolysis, and prolonged
activation of AMP-activated protein kinase, indicating metabolic stress. Muc1
clearly plays a significant role in enhancing the HIF protective pathway during
ischemic insult and recovery in kidney epithelia, providing a new target for
developing therapies to treat AKI. Moreover, our data support a role specifically
for HIF-1 in epithelial protection of the kidney during IRI as Muc1 is present
only in tubule epithelial cells.
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