Fig. 5: HDAC4 accelerates cell apoptosis by reducing miR-206 expression and activating the MEKK1/JNK axis in cardiomyocytes from IRI rats. | Cell Death Discovery

Fig. 5: HDAC4 accelerates cell apoptosis by reducing miR-206 expression and activating the MEKK1/JNK axis in cardiomyocytes from IRI rats.

From: Histone deacetylase HDAC4 participates in the pathological process of myocardial ischemia-reperfusion injury via MEKK1/JNK pathway by binding to miR-206

Fig. 5

Cardiomyocytes were transfected with oe-NC + NC mimic, oe-HDAC4 + NC mimic, oe-NC + miR-206 mimic, oe-HDAC4 + miR-206 mimic, miR-206 mimic + oe-NC, or miR-206 mimic + oe-MEKK1. A Expression of miR-206 in cardiomyocytes determined by RT-qPCR, normalized to U6. B Protein expression of HDAC4, MEKK1, JNK, p-JNK, Bax, cleaved Caspase-3, and Bcl-2 in cardiomyocytes determined by western blot analysis, normalized to GAPDH. C The levels of IL-6 and TNF-α in cardiomyocytes determined by ELISA. D Determination of SOD, GSH, and MDA contents in cardiomyocytes. E Apoptosis of cardiomyocytes detected by flow cytometry. Data were all measurement data and expressed as mean ± standard derivation. Comparisons among multiple groups were analyzed by one-way ANOVA, followed by Tukey’s host hoc test. *p < 0.05 vs. the cardiomyocytes co-transfected with oe-NC and NC mimic; #p < 0.05 vs. the cardiomyocytes co-transfected with oe-HDAC4 and NC; @p < 0.05 vs. the cardiomyocytes co-transfected with miR-206 mimic and oe-NC. The experiment was conducted three times independently.

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