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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+Transl+Res
2017 ; 9
(5
): 2412-2420
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Exogenous MSCs ameliorate hypoxia/reoxygenation injury in renal tubular
epithelial cells through JAK/STAT signaling pathway-mediated regulation of HMGB1
#MMPMID28559991
Zhang L
; Wang Y
; Ma J
; Lai X
; Fang J
; Li G
; Xu L
; Pan G
; Chen Z
Am J Transl Res
2017[]; 9
(5
): 2412-2420
PMID28559991
show ga
This study was conducted to investigate the repair mechanism of
hypoxia/reoxygenation injury (HRI) in renal tubular epithelial cells (HK-2) by
exogenous mesenchymal stem cells (MSCs). The activation of the JAK/STAT pathway
in HK-2 cells after HRI and treatment of MSCs, JAK inhibitor WP1066 and STAT
inhibitor SOCS3 was investigated using Western blot analysis. HK-2 cells were
transfected with siRNA STAT3 and analyzed for expression of STAT3, JAK2 and HMGB1
using fluorescence quantitative PCR and Western blot. Cell viability and
apoptosis were analyzed using the MTT assay and flow cytometry. After HRI, the
JAK/STAT pathway in HK-2 cells was activated, resulting in the upregulation of
JAK1, JAK2, JAK3, p-JAK1, p-JAK2, p-JAK3, STAT1, STAT2, STAT3, p-STAT1, p-STAT2
and p-STAT3. After treatment with MSC conditioned medium (MSCs CM), WP1066, or
SOCS, the expression of these proteins was significantly down-regulated. When the
cells were transfected with siRNA STAT3, the expression of STAT3 at protein and
mRNA levels and JAK2 and HMGB1 at mRNA level was down-regulated; the cell
viability was reduced and apoptosis increased. It is concluded that exogenous
MSCs reduce HRI of HK-2 cells by suppressing the JAK/STAT signaling pathway and
down-regulating the expression of HMGB1.