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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 PLoS+One
2016 ; 11
(2
): e0148821
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gab.com Text
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English Wikipedia
miRNA-221-3p Enhances the Secretion of Interleukin-4 in Mast Cells through the
Phosphatase and Tensin Homolog/p38/Nuclear Factor-kappaB Pathway
#MMPMID26901347
Zhou Y
; Yang Q
; Xu H
; Zhang J
; Deng H
; Gao H
; Yang J
; Zhao D
; Liu F
PLoS One
2016[]; 11
(2
): e0148821
PMID26901347
show ga
Mast cells play a central role in asthma. Moreover, serum miRNA-221-3p (miR-221)
has been shown to be markedly increased in children with asthma. In the current
study, we aimed to examine miR-221 expression in an asthma model and elucidate
the mechanisms regulating interleukin (IL)-4 secretion in mast cells. Using
polymerase chain reaction, we found that miR-221 was upregulated in a murine
asthma model and in P815 mast cells after lipopolysaccharide (LPS) stimulation.
Moreover, miR-221 upregulated IL-4 secretion from P815 cells, as shown by
enzyme-linked immunosorbent assays. Bioinformatics analysis, luciferase reporter
gene assays, and western blotting showed that phosphatase and tensin homolog
(PTEN) was a target of miR-221 and could block IL-4 secretion stimulated by
miR-221. The phosphorylation of p38 (protein) and activity of nuclear
factor-kappaB (NF-?B) were increased after overexpression of miR-221, as shown by
electrophoretic mobility shift assays. Finally, treatment with specific
inhibitors could block IL-4 secretion. In conclusion, miR-221, which was
overexpressed in a murine asthma model, stimulated IL-4 secretion in mast cells
through a pathway involving PTEN, p38, and NF-?B.