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Published on: February 24, 2017
Early Postnatal Cardiac Stress Does Not Influence Ventricular Cardiomyocyte Cell-Cycle Withdrawal
Marie Günthel1, Karel van Duijvenboden1, Jorn Jeremiasse1
1Academic Medical Center, Department of Medical Biology, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centers, 1100 DD Amsterdam, The Netherlands.
Insights
Congenital heart disease causes cardiac stress in newborns. This study found that while stress upregulates cell-cycle genes in neonatal cardiomyocytes, it does not affect their normal withdrawal from the cell cycle post-birth.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Genetics
Background:
- Congenital heart disease (CHD) is the most common birth defect, often leading to cardiac stress postnatally.
- The impact of this postnatal cardiac burden on ventricular development and adaptation remains poorly understood.
Purpose of the Study:
- To investigate the transcriptional and cell-cycle responses of neonatal cardiomyocytes to cardiac stress.
- To determine if induced cardiac stress affects postnatal cardiomyocyte cell-cycle withdrawal.
Main Methods:
- Utilized a genetic mouse model exhibiting left ventricular volume overload shortly after birth.
- Performed transcriptome analysis to assess gene expression changes.
- Quantified cell-cycle activity using Ki-67 immunostaining.
Main Results:
- Early upregulation of the cardiac stress marker Nppa was observed in the left ventricle and interventricular septum.
- Transcriptome analysis revealed induced expression of cell-cycle genes in response to cardiac stress.
- Despite gene expression changes, postnatal cell-cycle withdrawal in cardiomyocytes and other ventricular cells was not influenced.
Conclusions:
- Neonatal cardiac stress, even with increased cell-cycle gene expression, does not impede the normal process of cardiomyocyte cell-cycle withdrawal.
- This suggests a potential resilience in the neonatal heart's developmental program to certain stress-induced transcriptional changes.
Abstract:
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.
