ABSTRACT
ObjectiveMiRNA can regulate the occurrence and development of many inflammatory diseases, which is one of the hot spots in the research of inflammatory diseases. Bronchial asthma is a chronic inflammation, and the role of microRNA-19a in the regulation of bronchial asthma is still unclear. This paper discusses the expression changes of microRNA-19a /PI3K/AKT/PTEN pathway in rat asthma model.Methods(1) The rat model of chronic bronchial asthma was established. (2) The expression levels of AKT, p-AKT and PTEN in lung tissues were detected by western blot. (3) microRNA-19a expression in lung tissue of the model was detected by real-time fluorescence quantitative PCR.Results(1) HE, MASSON, PSA and immunohistochemistry of lung tissues in the model were combined to determine the successful establishment of the model of chronic bronchial asthma. (2) Western blot results showed that the expression levels of AKT (0.434±0.012) and p-AKT (1.086±0.026) in asthma group were higher than those in control group and demi group. The decreased expression of PTEN (0.371±0.007) was statistically significant (P<0.05). (3)The expression of microRNA-19a in the lung tissues of the asthmatic rat model was significantly increased in the asthma group (6.22±1.61) and in the gedi group (1.93±0.54). Pair-comparison between the three groups was statistically significant (P<0.05).ConclusionThe microRNA-19a /PI3K/AKT/PTEN pathway may be involved in the pathophysiological process of bronchial asthma.
ABSTRACT
AIM:TostudythefunctionofmicroRNA(miR)-19aandmiR-92abyseed-targetinginhibitionin multiple myeloma cells and their signal pathways .METHODS:The experiments were divided into t-antimiR-19a group, t-antimiR-92a group, scramble control group and blank control group .The growth-inhibitory potencies were measured by MTT assay.The ability of cell colony formation was measured by cell colony formation assay .The ability of cell invasion was measured by Transwell experiment .The miR-19a and miR-92a target gene signal pathways were integrated by miRFo-cus software.RESULTS:MTT assay showed that t-antimiR-19a and t-antimiR-92a significantly inhibited the viability of multiple myeloma cells , and the best concentration and time were 0.5μmol/L and 48 h, respectively .The colony number in t-antimiR-19a/92a group was less than that in scramble control group .The transfection with t-antimiR-19a or t-antimiR-92a effectively decreased the cell invasion , as the relative invasion cell number was significantly decreased compared with scramble control group.miR-19a and miR-92a were involved in mTOR signaling, cell cycle and other cancer pathways . CONCLUSION:miR-19a and miR-92a cluster might be a potential target for therapeutic intervention in multiple myelo-ma.
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[ ABSTRACT] AIM: To observe the effect of microRNA-19a ( miR-19a) on the lipid catabolism of hepatocyte LO2, and to explore the potential mechanism.METHODS: miR-19a was over-expressed or silenced by transfection of miR-19a mimics or miR-19a inhibitor into LO2 cells, then the mRNA level of miR-19a was detected by real-time PCR.The potential target of miR-19a was found by the method of bioinformatics through internet website.The effect of miR-19a on the 3’ UTR of peroxisome proliferator-activated receptorα(PPARα) was measured by dual luciferase reporter assay, and the protein level of PPARαand its 2 major downstream rate-limiting enzymes involved in lipid catabolism, acyl-coenzyme a dehydrogenase (ACADM) and carnitine palmitoyltransferase 1A ( CPT1A), were detected by Western blotting.Mean-while, the effect of miR-19a on the generation of ketone body was measured by beta-hydroxybutyric acid (β-OHB) detec-tion assay.RESULTS:The mRNA level of miR-19a was dramatically elevated by the transfection of miR-19a mimics, and sharply decreased by the transfection of miR-19a inhibitor (P<0.05).PPARαwas found as a potential target of miR-19a, and dual luciferase reporter assay and Western blotting confirmed the regulatory effect of miR-19a on the expression of PPARα, with the protein level changes of ACADM and CPT1A.miR-19a mimics down-regulated, while miR-19a inhibitor up-regulated the concentration ofβ-OHB in LO2 cells (P<0.05).CONCLUSION:miR-19a regulates the lipid catabo-lism of hepatocytes by targeting the PPARαand its 2 downstream rate-limiting enzymes.