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. 2021 Jan 1;11(6):3000–3016. doi: 10.7150/thno.47354

Figure 1.

Figure 1

Knock down of ALKBH5 inhibits cardiomyocyte proliferation. (A) m6A ELISA assay of mRNA isolated from P1 and P7 hearts. *P < 0.05, n = 3. (B) Western blot assay of ALKBH5 in hearts from P1, P7 and P10 mice. β-TUBULIN was used as a loading control. (C) RT-qPCR analysis of ALKBH5 in hearts from P1, P7 and P10 mice *P < 0.05, and ***P < 0.001 (n = 4). (D) RT-qPCR analysis of ALKBH5 of hearts harvested 4 days after an AR operation on a 1-day-old mice **p < 0.01 (n = 4). (E) RT-qPCR analysis of ALKBH5 in cultured cardiomyocytes transfected with three independent ALKBH5 siRNA and negative control siRNA (NC). ***p < 0.001 (n = 4). (F-K) Cardiomyocytes isolated from P1 mice were transfected with CTL-siRNA or ALKBH5-siRNA and immunostained against EdU, phospho-histone H3 (pH3), Aurora B kinase and α-actinin (marks cardiomyocytes). DAPI was used for nuclear staining. *P < 0.05, **P < 0.01, ***P < 0.001. n = 5 per group. The arrows point to EdU/pH3/Aurora B kinase-positive signal. Scale bar, 30 μm.