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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 Biochem+Biophys+Rep
2015 ; 2
(ä): 69-74
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English Wikipedia
Interleukin-6/STAT pathway is responsible for the induction of gene expression of
REG I?, a new auto-antigen in Sjögren?s syndrome patients, in salivary duct
epithelial cells
#MMPMID29124146
Fujimura T
; Fujimoto T
; Itaya-Hironaka A
; Miyaoka T
; Yoshimoto K
; Yamauchi A
; Sakuramoto-Tsuchida S
; Kondo S
; Takeda M
; Tsujinaka H
; Azuma M
; Tanaka Y
; Takasawa S
Biochem Biophys Rep
2015[Jul]; 2
(ä): 69-74
PMID29124146
show ga
The regenerating gene, Reg, was originally isolated from a rat regenerating islet
cDNA library, and its human homolog was named REG I?. Recently, we reported that
REG I? mRNA as well as its product were overexpressed in ductal epithelial cells
in the minor salivary glands of Sjögren?s syndrome (SS) patients. This study was
undertaken to elucidate the role of cytokines and the subsequent intracellular
mechanism for induction of REG I? in the salivary glands of SS patients. We
prepared a reporter plasmid containing REG I? promoter (-1190/+26) upstream of a
luciferase reporter gene. The promoter plasmid was introduced by lipofection into
human NS-SV-DC and rat A5 salivary ductal cells. The cells were treated with
interleukin (IL)-6, IL-8, and a combination of the two. Thereafter
transcriptional activity of REG I? was measured by luciferase assay. We found
that IL-6 stimulation, but not IL-8, significantly enhanced the REG I? promoter
activity in salivary ductal cells. Deletion analysis revealed that the region of
-141 to -117 of the REG I? gene was responsible for the promoter activation by
IL-6, which contains a consensus sequence for signal transduction and activation
of transcription (STAT). The introduction of siRNA for human STAT3 abolished
IL-6-induced REG I? transcription. These results showed that IL-6 stimulation
induced REG I? transcription through STAT3 activation and binding to the
consensus sequence of REG I? promoter in salivary ductal cells. This IL-6/STAT
dependent REG I? induction might play a role in the pathogenesis of SS.