Dynamic Variation of MiRNA-350 and JNK Signaling Pathway in Mice Cardiac throughout Cardiac Remodeling Induced to Exercise Training

Objective:Cardiac hypertrophy model was induced by increasing load treadmill exercise, in order to observe the dynamic variation of miRNA-350and target molecules in mice cardiac throughout a 8week's increasing loading training, and explore the possibly mechanism of cardiac remodeling exercise training.Methods:96 male C57BL/6 mice were randomly divided into 2groups named control group and increasing load group.The cardiac structural and function parameters of all mice were determined by the ultrasonic cardiogram at the end of 7th week during the formal exercise training.The dynamic alternations of miRNA-350during different time phases of cardiac remodeling induced to exercise training was determined by qRTPCR.The dynamic expression of JNK mRNA and JNK protein was determined by qRT-PCR and Western Blotting technology.Results:There were significantly differences in the sizes of PWTS, PWTD, LVEDD、IVSTD and IVSTS between the C group and group ILT, but no difference in the eject fraction.At first, the expression of miRNA-350in the cardiac of ILT group presented a sharp ascent and followed an acute decline, and then slowly down to a level similar to C group.At the day of 0, 3and 7throughout increasing load training period, the expression of JNK mRNA, target gene of miRNA-350had no remarkable change.Since then the expression level of JNK mRNA increased gradually.The expression of JNK protein decreased dramatically and then increased slowly in the course of cardiac remodeling induced by exercise.Conclusions:It indicated that a lasting 8weeks' increasing load treadmill exercise training induced a cardiac hypertrophy successfully.It appeared that the expression of miRNA-350, JNK mRNA and JNK protein showed a dynamic alternations during exercise-induced cardiac remodeling, and implied that miRNA-350/JNK signaling pathways possibly involved in the regulation of exercise-induced cardiac remodeling.