Regulation of the cardiomyocyte population in the developing heart

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    54 Citations (Scopus)

    Abstract

    During fetal life the myocardium expands through replication of cardiomyocytes. In sheep, cardiomyocytes begin the process of becoming terminally differentiated at about 100 gestation days out of 145 days term. In this final step of development, cardiomyocytes become binucleated and stop dividing. The number of cells at birth is important in determining the number of cardiomyocytes for life. Therefore, the regulation of cardiomyocyte growth in the womb is critical to long term disease outcome. Growth factors that stimulate proliferation of fetal cardiomyocytes include angiotensin II, cortisol and insulin-like growth factor-1. Increased ventricular wall stress leads to short term increases in proliferation but longer-term loss of cardiomyocyte generative capacity. Two normally circulating hormones have been identified that suppress proliferation: atrial natriuretic peptide (ANP) and tri-iodo-l-thyronine (T3). Atrial natriuretic peptide signals through the NPRA receptor that serves as a guanylate cyclase and signals through cGMP. ANP powerfully suppresses mitotic activity in cardiomyocytes in the presence of angiotensin II in culture. Addition of a cGMP analog has the same effect as ANP. ANP suppresses both the extracellular receptor kinases and the phosphoinositol-3 kinase pathways. T3 also suppresses increased mitotic activity of stimulated cardiomyocytes but does so by increasing the cell cycle suppressant, p21, and decreasing the cell cycle activator, cyclin D1.

    Original languageEnglish (US)
    Pages (from-to)289-299
    Number of pages11
    JournalProgress in Biophysics and Molecular Biology
    Volume106
    Issue number1
    DOIs
    StatePublished - Jul 2011

    Fingerprint

    Cardiac Myocytes
    Atrial Natriuretic Factor
    Population
    Angiotensin II
    Cell Cycle
    Phosphotransferases
    Thyronines
    Guanylate Cyclase
    Cyclin D1
    Somatomedins
    Hydrocortisone
    Sheep
    Intercellular Signaling Peptides and Proteins
    Myocardium
    Cell Count
    Parturition
    Hormones
    Pregnancy
    Growth

    Keywords

    • Atrial natriuretic peptide
    • Cardiomyocyte
    • Fetus
    • Programming
    • Terminal differentiation
    • Tri-iodo-l-thyronine

    ASJC Scopus subject areas

    • Molecular Biology
    • Biophysics

    Cite this

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    title = "Regulation of the cardiomyocyte population in the developing heart",
    abstract = "During fetal life the myocardium expands through replication of cardiomyocytes. In sheep, cardiomyocytes begin the process of becoming terminally differentiated at about 100 gestation days out of 145 days term. In this final step of development, cardiomyocytes become binucleated and stop dividing. The number of cells at birth is important in determining the number of cardiomyocytes for life. Therefore, the regulation of cardiomyocyte growth in the womb is critical to long term disease outcome. Growth factors that stimulate proliferation of fetal cardiomyocytes include angiotensin II, cortisol and insulin-like growth factor-1. Increased ventricular wall stress leads to short term increases in proliferation but longer-term loss of cardiomyocyte generative capacity. Two normally circulating hormones have been identified that suppress proliferation: atrial natriuretic peptide (ANP) and tri-iodo-l-thyronine (T3). Atrial natriuretic peptide signals through the NPRA receptor that serves as a guanylate cyclase and signals through cGMP. ANP powerfully suppresses mitotic activity in cardiomyocytes in the presence of angiotensin II in culture. Addition of a cGMP analog has the same effect as ANP. ANP suppresses both the extracellular receptor kinases and the phosphoinositol-3 kinase pathways. T3 also suppresses increased mitotic activity of stimulated cardiomyocytes but does so by increasing the cell cycle suppressant, p21, and decreasing the cell cycle activator, cyclin D1.",
    keywords = "Atrial natriuretic peptide, Cardiomyocyte, Fetus, Programming, Terminal differentiation, Tri-iodo-l-thyronine",
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    AU - Thornburg, Kent

    AU - Jonker, Sonnet

    AU - O'Tierney, Perrie

    AU - Chattergoon, Natasha

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    AU - Giraud, George

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