This study set out to explore the
potential role of microRNA-361-5p
(miR-361-5p) in acute pancreatitis through regulation of interleukin-17A
(IL-17A). We first identified the expression of miR-361-5p, IL-17A,
nuclear factor IA (NFIA), and hes family bHLH transcription factor
1 (Hes1) in serum samples collected from patients with acute pancreatitis,
caerulein-induced mice, and a Th17 cell model. The predicted binding
of miR-361-5p to NFIA was confirmed in vitro. Gain-
and loss-of-function assays of miR-361-5p and NFIA were employed to
elucidate their effects on acute pancreatitis. miR-361-5p promoted
Th17 cells to secrete IL-17A and then aggravated acute pancreatitis.
miR-361-5p directly targeted NFIA by binding to its promoter region,
leading to its downregulation. Overexpression of NFIA reduced Hes1
expression and rescued the promoting effect of miR-361-5p on IL-17A
secretion. In summary, miR-361-5p enhances IL-17A secretion from Th17
cells and thus aggravates acute pancreatitis by targeting NFIA and
upregulating Hes1.
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