fig2

Hypoxia-induced stabilization of HIF2A promotes cardiomyocyte proliferation by attenuating DNA damage

Figure 2. Ectopic HIF2A promotes cardiomyocyte proliferation and improves cardiac function after injury. (A and B) Representative pH3+ cardiomyocyte nucleus (white arrow) from a MCM;HIF2A-OE heart and quantification (scale bar 10 µm). (C and D) MADM quantification and tissue section images of single-labeled and double-labeled cells from control and MCM;HIF2A-OE tissue sections. Red and green arrows point to single-labeled CMs (scale bar 80 µm). (E and F) Baseline and post-injury ejection fraction of control and MCM;HIF2A-OE mice following adult LAD ligation-induced MI, along with representative M-mode echocardiographic images. (G and H) Mean percent fibrosis in control and MCM;HIF2A-OE hearts 12 weeks after injury using Masson trichrome staining and representative cross-sectional images. (I and J) Cell size in control and MCM;HIF2A-OE hearts 12 weeks after MI using WGA staining, along with representative images. MADM: Mosaic analysis with double markers; LAD: left anterior descending artery; OE: overexpression. Each dot represents one biological replicate. *P < 0.05 by unpaired t test in (E).

The Journal of Cardiovascular Aging

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Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/