Expression of miR-98 in myocarditis and its influence on transcription of the FAS/FASL gene pair.
Myocarditis is a common cardiovascular disease and frequently occurs in children and teenagers. It is believed to be caused by both endogenous and exogenous factors, among which FAS/FASL gene pair-induced cell apoptosis is a major mechanism of myocardial cell injury. A previous study has detected low expression of microRNA (miR)-98 in myocarditis patients. Therefore, in this study we investigated the functional implications of miR-98 with respect to the disease. We carried out a case-control study including 50 myocarditis patients and 50 healthy individuals. Total RNA was extracted from peripheral blood plasma. Expression levels of miR-98 and the FAS/FASL gene pair were determined by real-time fluorescent quantitative polymerase chain reaction. The interaction between miR-98 and the FAS/FASL pair was visualized by dual-luciferase reporter assay. The expression of the FAS/FASL gene pair was further detected by transfecting with an miR-98 mimic or an miR-98 inhibitor. The content of miR-98 in the peripheral blood of the myocarditis patients was significantly lower than in the healthy individuals. However, the FAS/FASL genes were upregulated by 1.68-fold in the myocarditis patients. miR-98 was shown to interact with the 3'-untranslated region of the FAS/FASL gene pair. The inhibition/facilitation of miR-98 expression in myocardial cells can modulate apoptosis. miR-98 was downregulated in the peripheral blood of myocarditis patients. It may interact with the FAS/FASL gene pair to further modulate cell apoptosis.
Department of Cardiology, Tianjin Nankai Hospital, Nankai, Tianjin, China.
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Zhang
Department of Toxicology, Tianjin Entry Exit Inspection and Quarantine Bureau, Dongli, Tianjin, China.
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Z
Zhao
Department of Clinical, Tianjin Nankai Hospital, Dongli, Tianjin, China.
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Z
Jin
D017209:Apoptosis / Q000235:genetics; D016022:Case-Control Studies; D053222:Fas Ligand Protein / Q000096:biosynthesis* / Q000235:genetics; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D009205:Myocarditis / Q000235:genetics* / Q000473:pathology; D009206:Myocardium / Q000473:pathology; D019014:fas Receptor / Q000096:biosynthesis* / Q000235:genetics
C491901:FAS protein, human; C505661:FASLG protein, human; D053222:Fas Ligand Protein; C546084:MIRN98 microRNA, human; D035683:MicroRNAs; D019014:fas Receptor