Journal
BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY
Volume 84, Issue 2, Pages 321-329Publisher
OXFORD UNIV PRESS
DOI: 10.1080/09168451.2019.1685370
Keywords
Microrna-210-3p; IGF2; macrophage; lipid accumulation; pro-inflammatory cytokine secretion
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Funding
- Natural Science Foundation research project of Shaanxi Province China [2014JM4127, 2012SF2-12]
- National Natural Science Foundation of China [81300226, 81500219, 81870330]
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Previous studies have shown that miR-210-3p is involved in the development and progression of atherosclerosis, but its specific mechanisms are still unclear. This study aims to reveal the mechanism of miR-210-3p and its target genes in macrophage lipid deposition and inflammatory response, and provide new ideas for the treatment of atherosclerosis. We found miR-210-3p increased sharply in the first 12 h induced by higher doses of ox-LDL in THP-1 macrophages and then gradually decreased. MiR-210-3p mimic transfection inhibited lipid uptake and inflammatory cytokine production in ox-LDL-induced macrophages. By inhibiting IGF2/IGF2R, miR-210-3p suppressed the expression of fatty acid transcriptase CD36 and transcription factor NF-kappa B in ox-LDL-induced macrophages. In conclusion, miR-210-3p inhibits the expression of CD36 and NF-kappa B by inhibiting IGF2 / IGF2R, thereby reducing lipid accumulation and inflammatory response in ox-LDL-induced macrophages. Enhancing miR-210-3p expression may be a new strategy for the treatment of atherosclerosis.
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