Aerobic exercise protects MI heart through miR-133a-3p downregulation of connective tissue growth factor

Figures

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  Fig 1. Experimental overview diagram for this article. One week after myocardial infarction surgery, all mice in the exercise group underwent aerobic exercise training on a small animal treadmill for 5 weeks. After exercise, all experimental mice were anesthetized using isoflurane and then subjected to neck-breaking execution in order to collect cardiac tissue and serum samples for subsequent experiments.

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  Fig 2. Aerobic exercise improves infarction-induced cardiac dysfunction. (A) Survival curve of mice in different groups, n = 8–10. Systolic and diastolic function of the left ventricle is assessed by measuring small animal ultrasound parameters, including (B) LVIDd, (C) LVIDs, (D) EF and (E) Ultrasound image acquisition (n = 6). Light microscope capture of Masson stained image with collage in the blue area, normal myocardial myofibrils in the red area, and nuclei in the dark brown area (scale bar = 0.61 μm). (F) Masson stained image capture results (G) Collagen volume fraction (CVF %) determined by digital measurement of Matson staining (n = 3). SE, S+ exercise group; S, sham group; MI, myocardial infarct group; ME, MI+ exercise group. *P<0.05, **P<0.01.

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  Fig 3. The expression of miR-133a-3p and CTGF in cardiac muscle. (A) miR-133a-3p mRNA expression in the heart (n = 3). (B) Western blotting results of CTGF protein in heart tissues (n = 3). (C) Western blot images of CTGF protein in infarct area and non-infarct area in different groups (n = 3). The values are presented as the mean ± SEM. SE, S+ exercise group; S, sham group; MI, myocardial infarct group; ME, MI+ exercise group. *P<0.05, **P<0.01.

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  Fig 4. The ameliorative effect of aerobic exercise on myocardial infarction-induced apoptosis in cardiomyocytes. (A, B) Western blotting results of apoptosis-related proteins Bax and Bcl-2 in myocardial tissues (n = 3). (C) BAX/Bcl-2 protein blotting ratio. (D-E) Relative activity of Caspase-3 and Cleaved Caspase-3 enzyme in myocardial tissue using enzyme markers (n = 6). The values are presented as the mean ± SEM. SE, S+ exercise group; S, sham group; MI, myocardial infarct group; ME, MI+ exercise group. *P<0.05, **P<0.01.

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  Fig 5. The expression of miR-133a-3p and CTGF in H9C2 cells. (A) H9C2 cells morphology under light microscope. (B) Quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis of miR-133a-3p expression in the H9C2 cells. (C) Western blot images of CTGF protein in H9C2 cells and densitometric analysis of the band. The values are presented as the mean ± SEM. *P<0.05, **P<0.01.

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  Fig 6. The expression of CTGF in miR-133a-3p inhibitor and mimics transfected H9C2 cells. (A) Transfection concentrations of miR-133a-3p inhibitor in H9C2 cells. (B) Transfection concentrations of miR-133a-3p mimics in H9C2 cells. (C) Expression of CTGF in H9C2 cells after transfection with miR-133a-3p inhibitor. (D) Expression of CTGF in H9C2 cells after transfection with miR-133a-3p mimics. The values are presented as the mean ± SEM. *P<0.05, **P<0.01.

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  Fig 7. The expression of apoptosis in miR-133a-3p inhibitor and miR-133a-3p mimics transfected H9C2 cells. (A) Expression of apoptosis in H9C2 cells after transfection with miR-133a-3p inhibitor. (B) Expression of apoptosis in H9C2 cells after transfection with miR-133a-3p mimics. The values are presented as the mean ± SEM. *P<0.05, **P<0.01.