Key result
LV volume overload upregulates cell-cycle genes but fails to alter cardiomyocyte cell-cycle withdrawal in neonatal mice.
Why the study?
It was unknown how cardiac stress resulting from abnormal loading conditions in congenital heart disease influences postnatal ventricular development and cardiomyocyte adaptation.
Does early postnatal cardiac stress influence ventricular cardiomyocyte cell-cycle withdrawal in a neonatal mouse model?
Does early postnatal cardiac stress influence ventricular cardiomyocyte cell-cycle withdrawal in a neonatal mouse model?
Early postnatal cardiac stress from volume overload upregulates stress and cell-cycle genes but does not alter the normal postnatal cell-cycle withdrawal of ventricular cardiomyocytes.
Stress does not alter withdrawal despite gene upregulation; leaves open therapeutic targeting of neonatal cardiomyocyte proliferation.
Congenital heart disease (CHD) is the most common birth defect. After birth, patients with CHD may suffer from cardiac stress resulting from abnormal loading conditions. However, it is not known how this cardiac burden influences postnatal development and adaptation of the ventricles. To study the transcriptional and cell-cycle response of neonatal cardiomyocytes to cardiac stress, we used a genetic mouse model that develops left ventricular volume overload within 2 weeks after birth. The increased volume load caused upregulation of the cardiac stress marker Nppa in the left ventricle and interventricular septum as early as 12 days after birth. Transcriptome analysis revealed that cardiac stress induced the expression of cell-cycle genes. This did not influence postnatal cell-cycle withdrawal of cardiomyocytes and other cell types in the ventricles as measured by Ki-67 immunostaining.
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Günthel et al. (2021) studied Left ventricular volume overload / Congenital heart disease. Left ventricular volume overload (cardiac stress) vs. Healthy control mice was evaluated on Cardiomyocyte cell-cycle activity (percentage of Ki-67 positive cardiomyocyte nuclei). Early postnatal cardiac stress induced by left ventricular volume overload upregulated cell-cycle genes but did not alter the rate of cardiomyocyte cell-cycle withdrawal in neonatal mice.
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