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Silence of long intergenic noncoding RNA HOTAIR ameliorates oxidative stress and inflammation response in ox‐LDL‐treated human macrophages by upregulating miR‐330‐5p
Author(s) -
Liu Jie,
Huang GuangQing,
Ke ZunPing
Publication year - 2019
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.27317
Subject(s) - hotair , oxidative stress , long non coding rna , inflammation , intergenic region , silence , rna , biology , cancer research , microbiology and biotechnology , gene , immunology , genetics , biochemistry , genome , philosophy , aesthetics
Abstract Evidence of the involvement of long noncoding RNAs (lncRNAs) in atherosclerosis is growing but still not well characterized. Here, we concentrated on the biological roles of lncRNA HOX transcription antisense RNA (HOTAIR) in atherosclerosis. In our study, we found that oxidized low‐density lipoprotein (ox‐LDL) induced human macrophages THP‐1 cells apoptosis dose dependently and time dependently. Meanwhile, HOTAIR was significantly increased in THP‐1 cells treated with ox‐LDL. Then, HOTAIR was modulated by infection of LV‐short hairpin RNA (shRNA) and LV‐HOTAIR into THP‐1 cells. As displayed, CD36, Oil Red O staining levels, total cholesterol, triglyceride levels and dil‐ox‐LDL uptake rate were greatly repressed by the silence of HOTAIR while triggered by overexpression of HOTAIR. Moreover, knockdown of HOTAIR suppressed reactive oxygen species, malondialdehyde levels, increased superoxide dismutase activity and cell apoptosis were also restrained. Reversely, overexpression of HOTAIR exhibited an opposite phenomenon. In addition, interleukin 6 (IL‐6), IL‐1β, cyclo‐oxygenase 2, and tumor necrosis factor α protein levels were significantly depressed by LV‐shRNA) of HOTAIR while increased by upregulation of HOTAIR in THP‐1 cells. By carrying out bioinformatics analysis, miR‐330‐5p was predicted as a target of HOTAIR and the correlation between them was validated in our current study. MiR‐330‐5p was greatly decreased in THP‐1 cells incubated with ox‐LDL and overexpression of miR‐330‐5p was able to inhibit oxidative stress and inflammation process. Taken together, it was implied that HOTAIR contributed to atherosclerosis development by downregulating miR‐330‐5p in human macrophages.