LncRNA MEG3 aggravates palmitate-induced insulin resistance by regulating miR-185-5p/Egr2 axis in hepatic cells

被引:3
作者
Chen, D-L [1 ]
Shen, D-Y [2 ]
Han, C-K [3 ]
Tian, Y. [1 ]
机构
[1] Xiamen Univ, Zhongshan Hosp, Dept Endocrinol & Metab, Xiamen, Fujian, Peoples R China
[2] Xiamen Univ, Affiliated Hosp 1, Dept Biobank, Xiamen, Fujian, Peoples R China
[3] Xiamen Univ, Affiliated Hosp 1, Dept Radiol, Xiamen, Fujian, Peoples R China
关键词
LncRNA MEG3; miR-185-5p; Egr2; Hepatic insulin resistance; NONCODING RNA MEG3; METABOLIC SYNDROME; HEPG2; CELLS; EXPRESSION; PROLIFERATION; INFLAMMATION; JNK; OVEREXPRESSION; CARCINOMA; INSIGHTS;
D O I
暂无
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: Long non-coding RNA (LncRNA) has been reported to play an important role in type 2 diabetes (T2D). We investigated the role of LncRNA maternally expressed gene 3 (MEG3) and its potential interaction with miR-185-5p in palmitate-induced hepatocyte insulin resistance. PATIENTS AND METHODS: High-fat diet (HFD) mice and insulin resistant hepatocyte were employed. Relative mRNA expressions of MEG3, miR-185-5p, and early growth response proteins-2 (Egr2) were measured by qRT-PCR, Western blot was performed to evaluate Egr2 protein expression levels. Glycogen contents and plasma insulin levels were tested by the corresponding assay. RESULTS: MEG3 and Egr2 were upregulated. but miR-185-5p was downregulated in palmitate-treated insulin resistance hepatocytes and HFD mice. MEG3 knockdown alleviated the influence of palmitate on insulin resistance in vitro and in vivo. miR-185-5p expression was upregulated upon MEG3 knockdown. Expression of Egr2 was positively correlated with MEG3 knockdown or overexpression, which could be negatively managed by abnormal expression of miR-185-5p. CONCLUSIONS: Our data demonstrated that LncRNA MEG3 aggravated palmitate-induced insulin resistance by regulating miR-185-5p/Egr2 axis. providing new insights into T2D therapeutic strategies.
引用
收藏
页码:5456 / 5467
页数:12
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