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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 ; 309
(6
): F551-8
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MicroRNA-150 deletion in mice protects kidney from myocardial infarction-induced
acute kidney injury
#MMPMID26109086
Ranganathan P
; Jayakumar C
; Tang Y
; Park KM
; Teoh JP
; Su H
; Li J
; Kim IM
; Ramesh G
Am J Physiol Renal Physiol
2015[Sep]; 309
(6
): F551-8
PMID26109086
show ga
Despite greater understanding of acute kidney injury (AKI) in animal models, many
of the preclinical studies are not translatable. Most of the data were derived
from a bilateral renal pedicle clamping model with warm ischemia. However,
ischemic injury of the kidney in humans is distinctly different and does not
involve clamping of renal vessel. Permanent ligation of the left anterior
descending coronary artery model was used to test the role of microRNA (miR)-150
in AKI. Myocardial infarction in this model causes AKI which is similar to human
cardiac bypass surgery. Moreover, the time course of serum creatinine and
biomarker elevation were also similar to human ischemic injury. Deletion of
miR-150 suppressed AKI which was associated with suppression of inflammation and
interstitial cell apoptosis. Immunofluorescence staining with endothelial marker
and marker of apoptosis suggested that dying cells are mostly endothelial cells
with minimal epithelial cell apoptosis in this model. Interestingly, deletion of
miR-150 also suppressed interstitial fibrosis. Consistent with protection,
miR-150 deletion causes induction of its target gene insulin-like growth factor-1
receptor (IGF-1R) and overexpression of miR-150 in endothelial cells
downregulated IGF-1R, suggesting miR-150 may mediate its detrimental effects
through suppression of IGF-1R pathways.