ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Unexpected maturation of PI3K and MAPK-ERK signaling in fetal ovine cardiomyocytes.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 26 citations in OpenAlex.
- miR-203 improves pressure overload-induced heart failure by targeting the IGFBP5/PI3K/AKT axis.Acta pharmacologica Sinica · 2026Article
- Lipid exposure leads to metabolic dysfunction in fetal sheep cardiomyocytes.Physiological reports · 2025Article
- An overview of the multi-dimensional mechanisms of exercise-regulated hormones and growth factors in cardiac physiological adaptation.Frontiers in physiology · 2025Review
- Fetal cardiac troponin I levels decline toward birth in sheep.American journal of physiology. Heart and circulatory physiology · 2024Article
- Thyroid hormone increases fatty acid use in fetal ovine cardiac myocytes.Physiological reports · 2023Article
- Synergistic effects of hormones on structural and functional maturation of cardiomyocytes and implications for heart regeneration.Cellular and molecular life sciences : CMLS · 2023Review
- Article
- Mechanotransduction regulates inflammation responses of epicardial adipocytes in cardiovascular diseases.Frontiers in endocrinology · 2022Review
- Effect of Preterm Birth on Cardiac and Cardiomyocyte Growth and the Consequences of Antenatal and Postnatal Glucocorticoid Treatment.Journal of clinical medicine · 2021Review
- Coronary vascular growth matches IGF-1-stimulated cardiac growth in fetal sheep.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Thyroid hormone signaling and consequences for cardiac development.The Journal of endocrinology · 2019Review
- Thyroid hormone receptor function in maturing ovine cardiomyocytes.The Journal of physiology · 2019Article
- Cardiac myocyte proliferation and maturation near term is inhibited by early gestation maternal testosterone exposure.American journal of physiology. Heart and circulatory physiology · 2018Article
- Atrial ERK1/2 activation in the embryo leads to incomplete Septal closure: a novel mouse model of atrial Septal defect.Journal of biomedical science · 2017Article
- Hypothyroidism in utero stimulates pancreatic beta cell proliferation and hyperinsulinaemia in the ovine fetus during late gestation.The Journal of physiology · 2017Article
- Understanding cardiomyocyte proliferation: an insight into cell cycle activity.Cellular and molecular life sciences : CMLS · 2017Review
- Electrical and mechanical stimulation of cardiac cells and tissue constructs.Advanced drug delivery reviews · 2016Review
- Repair Injured Heart by Regulating Cardiac Regenerative Signals.Stem cells international · 2016Review
- Endocrine and other physiologic modulators of perinatal cardiomyocyte endowment.The Journal of endocrinology · 2016Review
- The programming of cardiovascular disease.Journal of developmental origins of health and disease · 2015Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
In the first two-thirds of gestation, ovine fetal cardiomyocytes undergo mitosis to increase cardiac mass and accommodate fetal growth. Thereafter, some myocytes continue to proliferate while others mature and terminally differentiate into binucleated cells. At term (145 days gestational age; dGA) about 60% of cardiomyocytes become binucleated and exit the cell cycle under hormonal control. Rising thyroid hormone (T3) levels near term (135 dGA) inhibit proliferation and stimulate maturation. However, the degree to which intracellular signaling patterns change with age in response to T3 is unknown. We hypothesized that in vitro activation of ERK, Akt, and p70(S6K) by two regulators of cardiomyocyte cell cycle activity, T3 and insulin like growth factor-1 (IGF-1), would be similar in cardiomyocytes at gestational ages 100 and 135 dGA. IGF-1 and T3 each independently stimulated phosphorylation of ERK, Akt, and p70(S6K) in cells at both ages. In the younger mononucleated myocytes, the phosphorylation of ERK and Akt was reduced in the presence of IGF-1 and T3. However, the same hormone combination led to a dramatic twofold increase in the phosphorylation of these signaling proteins in the 135 dGA cardiomyocytes-even in cells that were not proliferating. In the older cells, both mono- and binucleated cells were affected. In conclusion, fetal ovine cardiomyocytes undergo profound maturation-related changes in signaling in response to T3 and IGF-1, but not to either factor alone. Differences in age-related response are likely to be related to milestones in fetal cardiac development as the myocardium prepares for ex utero life.
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Registered trials
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