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Polyinosinic‐polycytidylic acid accelerates intestinal stem cell proliferation via modulating Myc expression
Author(s) -
Zeng Huihong,
Tang Jiahui,
Yue Mengzhen,
Cheng Jiaoqi,
Fan Ying,
Li Manjun,
Zhang Xinxin,
Li Huan,
Duan Hongyi,
Zhang Minqing,
Fan Guangqin,
Zhu Qingxian,
Shao Lijian
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29254
Subject(s) - crypt , tlr3 , jejunum , biology , stem cell , small intestine , enteroendocrine cell , enterocyte , microbiology and biotechnology , intestinal mucosa , chemistry , immunology , medicine , endocrinology , immune system , toll like receptor , endocrine system , innate immune system , hormone
It is well known that exposure of double‐stranded RNA (dsRNA) to intestine immediately induces villus damage with severe diarrhea, which is mediated by toll‐like receptor 3 signaling activation. However, the role of intestinal stem cells (ISCs) remains obscure during the pathology. In the present study, polyinosinic‐polycytidylic acid (poly[I:C]), mimicking viral dsRNA, was used to establish intestinal damage model. Mice were acutely and chronically exposed to poly(I:C), and ISCs in jejunum were analyzed. The results showed that the height of villus was shorter 48 hr after acute poly(I:C) exposure compared with that of controls, while chronic poly(I:C) treatment increased both villus height and crypt depth in jejunum compared with control animals. The numbers of ISCs in jejunum were significantly increased after acute and chronic poly(I:C) exposure. Poly (I:C)‐stimulated ISCs have stronger capacities to differentiate into intestine endocrine cells. Mechanistically, poly(I:C) treatment increased expression of Stat1 and Axin2 in the intestinal crypt, which was along with increased expression of Myc, Bcl2, and ISC proliferation. These findings suggest that dsRNA exposure could induce ISC proliferation to ameliorate dsRNA‐induced intestinal injury.