miR-152通过抑制低密度脂蛋白受体表达减少肝细胞的脂质摄取
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湖南省自然科学基金资助项目(14JJ2091);湖南省教育厅资助科研项目(12C0339)


MiR-152 Inhibits Hepatocyte Lipid Uptake by Targeting Low Density Lipoprotein Receptor
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    目的 探讨miR-152对HepG2细胞低密度脂蛋白受体(LDLR)表达及其脂质摄取能力的影响。方法生物信息学预测miR-152与LDLR 3’UTR的结合关系,荧光素酶报告基因检测miR-152与LDLR的结合情况。HepG2细胞中转染miR-152 mimic或inhibitor后,Western Blot检测LDLR 蛋白水平,油红O染色观察HepG2细胞内脂滴情况。结果 生物信息学预测表明miR-152与人LDLR 3’UTR的872-878位结合,且二者结合的自由能较低。miR-152显著抑制荧光素酶的活性及HepG2细胞LDLR蛋白的表达。miR-152明显抑制HepG2细胞对脂质的摄取,而anti-miR-152则刚好出现相反的结果。结论 miR-152通过沉默LDLR表达抑制肝细胞的脂质摄取。

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    Aim To explore the effect of miR-152 on low density lipoprotein receptor (LDLR) expression and hepatocyte lipid uptake. Methods Bioinformatics websites predicted the combination of miR-152 with LDLR 3’UTR. Luciferase reporter assay confirmed the binding of miR-152 to LDLR 3’UTR. LDLR expression was measured by Western Bolt,and intracellular lipid droplet stained with oil red O in HepG2 cells transfected miR-152 mimic and inhibitor. Results MiR-152 was bound to the 872-878 sites within human LDLR 3’UTR,furthermore,their binding free energy was very low. MiR-152 obviously inhibited the luciferase activity and hepatocyte LDLR expression. Lipid uptake was dramatically suppressed in HepG2 cells treated with miR-152. The exactly opposite results were observed by anti-miR-152 treatment. Conclusions MiR-152 targets LDLR expression and inhibits hepatocyte lipid uptake.

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方 勇,曾海燕,吕运成. miR-152通过抑制低密度脂蛋白受体表达减少肝细胞的脂质摄取[J].中国动脉硬化杂志,2015,23(08):774~778.

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  • 收稿日期:2015-04-28
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  • 在线发布日期: 2015-07-21