TY - JOUR
T1 - Early postnatal cardiac stress does not influence ventricular cardiomyocyte cell-cycle withdrawal
AU - Günthel, Marie
AU - van Duijvenboden, Karel
AU - Jeremiasse, Jorn
AU - van den Hoff, Maurice J. B.
AU - Christoffels, Vincent M.
N1 - Funding Information: Funding: This research was funded by Netherlands Heart Foundation COBRA3 to V.M.C. Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
PY - 2021
Y1 - 2021
N2 - 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.
AB - 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.
KW - Cardiomyocyte cell-cycle
KW - Congenital heart defect
KW - Neonatal heart
KW - Volume overload
UR - http://www.scopus.com/inward/record.url?scp=85104624040&partnerID=8YFLogxK
U2 - https://doi.org/10.3390/jcdd8040038
DO - https://doi.org/10.3390/jcdd8040038
M3 - Article
C2 - 33917189
SN - 2308-3425
VL - 8
JO - Journal of cardiovascular development and disease
JF - Journal of cardiovascular development and disease
IS - 4
M1 - 38
ER -