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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
2016 ; 8
(2
): 981-92
Nephropedia Template TP
gab.com Text
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Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for
lipopolysaccharide-induced acute lung injury mice
#MMPMID27158384
Jia CE
; Jiang D
; Dai H
; Xiao F
; Wang C
Am J Transl Res
2016[]; 8
(2
): 981-92
PMID27158384
show ga
OBJECTIVE: The aim of this study is to evaluate the role of pendrin in acute lung
injury (ALI)/acute respiratory distress syndrome (ARDS) and to explore whether
pendrin expression existing on alveolar cells. METHODS: ALI C57BL/6 mice model
induced by lipopolysaccharide (LPS) was established. The expression of pendrin in
lung was analyzed by RT-PCR and western blotting methods, the changes of lung
inflammatory parameters and pathology were observed, the cellular distribution of
pendrin in the lung was determined using immunofluorescence. Statistical
comparisons between groups were made by two-tailed Student's t-test. RESULTS:
Enhanced expression of the slc26a4 gene and production of pendrin in lungs of
LPS-induced ALI mice were confirmed. In comparison with vehicle-control mice,
methazolamide treatment mitigated lung inflammatory parameters and pathology.
IL-6 and MCP-1 in lung tissues and BALF in methazolamide-treated mice were
statistically decreased. Methazolamide treatment had significant effect on the
total protein concentration in the BALF and the ratio of lung wet/dry weight. The
percentage of macrophages in the BALF was increased. There was a low expression
of pendrin in ATII. CONCLUSIONS: Pendrin may be involved in pathological process
of LPS-induced ALI. Inhibition of the pendrin function could be used to treat
ALI. Airway epithelial cell may be a valuable therapeutic target for discovering
and developing new drugs and/or new therapeutic strategies for the treatment of
ALI/ARDS.