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Interleukin-10 control of pre-miR155 maturation involves CELF2.


ABSTRACT: The anti-inflammatory cytokine interleukin-10 (IL10) is essential for attenuating inflammatory responses, which includes reducing the expression of pro-inflammatory microRNA-155 (miR155) in lipopolysaccharide (LPS) activated macrophages. miR155 enhances the expression of pro-inflammatory cytokines such as TNF? and suppresses expression of anti-inflammatory molecules such as SHIP1 and SOCS1. We previously found that IL10 interfered with the maturation of pre-miR155 to miR155. To understand the mechanism by which IL10 interferes with pre-miR155 maturation we isolated proteins that associate with pre-miR155 in response to IL10 in macrophages. We identified CELF2, a member of the CUGBP, ELAV-Like Family (CELF) family of RNA binding proteins, as protein whose association with pre-miR155 increased in IL10 treated cells. CRISPR-Cas9 mediated knockdown of CELF2 impaired IL10's ability to inhibit both miR155 expression and TNF? expression.

SUBMITTER: Yoon JSJ 

PROVIDER: S-EPMC7179890 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Interleukin-10 control of pre-miR155 maturation involves CELF2.

Yoon Jeff S J JSJ   Wu Mike K MK   Zhu Tian Hao TH   Zhao Helen H   Cheung Sylvia T ST   Chamberlain Thomas C TC   Mui Alice L-F AL  

PloS one 20200423 4


The anti-inflammatory cytokine interleukin-10 (IL10) is essential for attenuating inflammatory responses, which includes reducing the expression of pro-inflammatory microRNA-155 (miR155) in lipopolysaccharide (LPS) activated macrophages. miR155 enhances the expression of pro-inflammatory cytokines such as TNFα and suppresses expression of anti-inflammatory molecules such as SHIP1 and SOCS1. We previously found that IL10 interfered with the maturation of pre-miR155 to miR155. To understand the me  ...[more]

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