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MiR‐181a inhibits vascular inflammation induced by ox‐LDL via targeting TLR4 in human macrophages
Author(s) -
Du XianJin,
Lu JingMin,
Sha Yin
Publication year - 2018
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.26622
Subject(s) - inflammation , cd36 , tlr4 , apoptosis , foam cell , microrna , cell , cell growth , cancer research , chemistry , microbiology and biotechnology , biology , immunology , macrophage , receptor , biochemistry , gene , in vitro
Atherosclerosis is a kind of chronic inflammation disease with lipid accumulation in in blood vessel linings. Increasing evidence has reported that microRNAs can exert crucial roles in atherosclerosis. In previous study, miR‐181a has been implicated to be abnormally expressed in atherosclerosis mice, however its detailed function in atherosclerosis remains uninvestigated. Hence, in our current study, we focused on the biological role of miR‐181a in atherosclerosis progression. Ox‐LDL has been commonly identified as an important atherosclerosis regulator. We observed that ox‐LDL induced THP‐1 cell apoptosis dose‐dependently and time‐ dependently. Meanwhile, 25 µg/ml ox‐LDL can promote foam cell formation and increased miR‐181a expression significantly. CD36 has been involved in atherosclerosis progression and it was found that overexpression of miR‐181a inhibited its protein levels. Moreover, miR‐181a mimics repressed foam cell formation, TC and TG levels induced by ox‐LDL dramatically. In addition, miR‐181a mimics were able to reverse THP‐1 cell apoptosis, increased IL‐6, IL‐1β, and TNF‐α protein expression triggered by 25 µg/ml ox‐LDL. TLR4 has been linked to various inflammation‐associated diseases. In our present study, TLR4 was indicated as miR‐181a target and the binding correlation between them was validated by dual‐luciferase reporter assay. In conclusion, these results improves the understanding of atherosclerosis modulated by miR‐181a/TLR4 and can contribute to development of new approaches for atherosclerosis.