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Interleukin-10 control of pre-miR155 maturation involves CELF2
Jeff S J Yoon1,2,3, Mike K Wu1,2,3, Tian Hao Zhu3
1Immunity and Infection Research Centre, Vancouver Coastal Health Research Institute, Vancouver, Canada.
Plos One
|April 24, 2020
Summary
Interleukin-10 (IL10) reduces inflammation by inhibiting microRNA-155 (miR155) maturation. This involves the RNA binding protein CELF2, which is crucial for IL10
Area of Science:
- Immunology
- Molecular Biology
- Gene Regulation
Background:
- Interleukin-10 (IL10) is a key anti-inflammatory cytokine.
- IL10 suppresses pro-inflammatory responses, including microRNA-155 (miR155) expression in macrophages.
- miR155 promotes inflammation by upregulating TNFα and downregulating SHIP1 and SOCS1.
Purpose of the Study:
- To elucidate the mechanism by which IL10 inhibits pre-miR155 maturation.
- To identify proteins interacting with pre-miR155 upon IL10 stimulation in macrophages.
Main Methods:
- Macrophage culture and stimulation with lipopolysaccharide (LPS) and IL10.
- Isolation of proteins associated with pre-miR155.
- CRISPR-Cas9 mediated knockdown of candidate proteins.
- Quantitative assessment of miR155, TNFα, SHIP1, and SOCS1 expression.
Main Results:
- CELF2 (CUGBP, ELAV-Like Family member 2) was identified as a protein associating with pre-miR155 in IL10-treated macrophages.
- IL10 treatment increased the association of CELF2 with pre-miR155.
- Knockdown of CELF2 using CRISPR-Cas9 abolished IL10's inhibitory effect on miR155 and TNFα expression.
Conclusions:
- CELF2 is a critical mediator of IL10's anti-inflammatory function.
- IL10 utilizes CELF2 to interfere with pre-miR155 maturation, thereby suppressing pro-inflammatory cytokine production.
- Targeting the IL10-CELF2-miR155 axis may offer therapeutic strategies for inflammatory diseases.
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