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

Figure 2.

Figure 2

Overexpression of ALKBH5 promotes cardiomyocyte proliferation. (A) Neonatal P1 cardiomyocytes were transfected with CTL-plasmids or ALKBH5-overexpression plasmids for 48 hr. CMs were immunostained against EdU, phospho-histone H3 (pH3), Aurora B kinase and α-actinin (marks cardiomyocytes). DAPI was used for nuclear staining. n = 5 per group. *P < 0.05, **P < 0.01, ***P < 0.001. The arrows point to EdU/pH3/Aurora B kinase-positive signal. Scale bar, 30 μm. (B) Isolated P7 cardiomyocytes were transfected with CTL-plasmids or ALKBH5-overexpression plasmids for 48 hr. CMs were immunostained against EdU, phospho-histone H3 (pH3), Aurora B kinase and α-actinin (marks cardiomyocytes). DAPI was used for nuclear staining. n = 5 per group. *P < 0.05, **P < 0.01, ***P < 0.001. The arrows point to EdU/pH3/Aurora B kinase-positive signal. Scale bar, 30 μm. (C) The effect of ALKBH5 on apoptosis of P1 cardiomyocytes as determined by TUNEL staining (n = 4).