心臓と肺のリハビリテーションのジャーナル

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HepG2 Expression of miR-202 and TRIB-1 under Metabolic and Inflammatory Stress

Iquo O. Phillip

Background: The burden of Cardiovascular Disease (CVD) is such that affects both developed and developing countries with high rates of mortality and morbidity. Cardiovascular diseases are highly polymorphic across its various risk factors. Human polymorphisms of Trib-1 gene have been implicated to be associated with risk factors for CVD. Trib-1 gene is a known target for microRNA-202 which consequently could have an effect on its stability. The objective of this study was to evaluate the expression of miR-202 in a hepatic cell line under in vitro conditions of metabolic and inflammatory stress and the effect on Trib-1 level.

Methodology: HepG2 cells cultured under in vitro conditions of high glucose and cytokine stimulation of concentrations of varying time intervals were harvested and mRNA/microRNA extracted using the spin columnbased centrifugation, reversed transcribed and analysed for endogenous expressions of Trib-1 and miR-202 using qPCR. One-ANOVA followed by Dunnett’s multiple comparison tests was used to test for significance (P<0.05) across samples.

Results: It was observed that there was a significant decrease in Trib-1 levels under these conditions of high glucose and cytokine stimulation and also with the combination of both whilst there was a consistent pattern of upregulation of miR-202 under this conditions.

Conclusion: Taken together this study reveals that miR-202 is expressed in HepG2 cells, and a possible interaction between Trib-1 and miR-202 which could affect Trib-1 stability and also the potentials for miR-202 to be involved in some cellular activities in HepG2 cells relating to these conditions.