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  1. Article: Cardiac myocyte cell cycle control in development, disease, and regeneration.

    Ahuja, Preeti / Sdek, Patima / MacLellan, W Robb

    Physiological reviews

    2007  Volume 87, Issue 2, Page(s) 521–544

    Abstract: ... In this review, we summarize the current understanding of cardiomyocyte cell cycle control in normal development ... as well as feasibility of therapeutic manipulation of the cardiac myocyte cell cycle for cardiac ... that the heart is a terminally differentiated organ and opened new prospects for cardiac regeneration ...

    Abstract Cardiac myocytes rapidly proliferate during fetal life but exit the cell cycle soon after birth in mammals. Although the extent to which adult cardiac myocytes are capable of cell cycle reentry is controversial and species-specific differences may exist, it appears that for the vast majority of adult cardiac myocytes the predominant form of growth postnatally is an increase in cell size (hypertrophy) not number. Unfortunately, this limits the ability of the heart to restore function after any significant injury. Interest in novel regenerative therapies has led to the accumulation of much information on the mechanisms that regulate the rapid proliferation of cardiac myocytes in utero, their cell cycle exit in the perinatal period, and the permanent arrest (terminal differentiation) in adult myocytes. The recent identification of cardiac progenitor cells capable of giving rise to cardiac myocyte-like cells has challenged the dogma that the heart is a terminally differentiated organ and opened new prospects for cardiac regeneration. In this review, we summarize the current understanding of cardiomyocyte cell cycle control in normal development and disease. In addition, we also discuss the potential usefulness of cardiomyocyte self-renewal as well as feasibility of therapeutic manipulation of the cardiac myocyte cell cycle for cardiac regeneration.
    MeSH term(s) Animals ; Cardiomegaly/physiopathology ; Cell Cycle/physiology ; Cell Proliferation ; Heart/growth & development ; Heart Diseases/pathology ; Heart Diseases/physiopathology ; Humans ; Myocytes, Cardiac/physiology ; Regeneration/physiology
    Language English
    Publishing date 2007-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 209902-0
    ISSN 1522-1210 ; 0031-9333
    ISSN (online) 1522-1210
    ISSN 0031-9333
    DOI 10.1152/physrev.00032.2006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: MBNL1 Regulates Programmed Postnatal Switching Between Regenerative and Differentiated Cardiac States.

    Bailey, Logan R J / Bugg, Darrian / Reichardt, Isabella M / Ortaç, C Dessirée / Nagle, Abigail / Gunaje, Jagadambika / Martinson, Amy / Johnson, Richard / MacCoss, Michael J / Sakamoto, Tomoya / Kelly, Daniel P / Regnier, Michael / Davis, Jennifer

    Circulation

    2024  Volume 149, Issue 23, Page(s) 1812–1829

    Abstract: ... myocyte proliferation and regeneration and MBNL1 deletion promoted regenerative states with prolonged ... by stabilizing adult myocyte mRNAs during postnatal development and throughout adulthood. Targeting loss ... cardiomyocyte cell cycle entry and proliferation through altered cell cycle inhibitor transcript stability ...

    Abstract Background: Discovering determinants of cardiomyocyte maturity is critical for deeply understanding the maintenance of differentiated states and potentially reawakening endogenous regenerative programs in adult mammalian hearts as a therapeutic strategy. Forced dedifferentiation paired with oncogene expression is sufficient to drive cardiac regeneration, but elucidation of endogenous developmental regulators of the switch between regenerative and mature cardiomyocyte cell states is necessary for optimal design of regenerative approaches for heart disease. MBNL1 (muscleblind-like 1) regulates fibroblast, thymocyte, and erythroid differentiation and proliferation. Hence, we examined whether MBNL1 promotes and maintains mature cardiomyocyte states while antagonizing cardiomyocyte proliferation.
    Methods: MBNL1 gain- and loss-of-function mouse models were studied at several developmental time points and in surgical models of heart regeneration. Multi-omics approaches were combined with biochemical, histological, and in vitro assays to determine the mechanisms through which MBNL1 exerts its effects.
    Results: MBNL1 is coexpressed with a maturation-association genetic program in the heart and is regulated by the MEIS1/calcineurin signaling axis. Targeted MBNL1 overexpression early in development prematurely transitioned cardiomyocytes to hypertrophic growth, hypoplasia, and dysfunction, whereas loss of MBNL1 function increased cardiomyocyte cell cycle entry and proliferation through altered cell cycle inhibitor transcript stability. Moreover, MBNL1-dependent stabilization of estrogen-related receptor signaling was essential for maintaining cardiomyocyte maturity in adult myocytes. In accordance with these data, modulating MBNL1 dose tuned the temporal window of neonatal cardiac regeneration, where increased MBNL1 expression arrested myocyte proliferation and regeneration and MBNL1 deletion promoted regenerative states with prolonged myocyte proliferation. However, MBNL1 deficiency was insufficient to promote regeneration in the adult heart because of cell cycle checkpoint activation.
    Conclusions: Here, MBNL1 was identified as an essential regulator of cardiomyocyte differentiated states, their developmental switch from hyperplastic to hypertrophic growth, and their regenerative potential through controlling an entire maturation program by stabilizing adult myocyte mRNAs during postnatal development and throughout adulthood. Targeting loss of cardiomyocyte maturity and downregulation of cell cycle inhibitors through MBNL1 deletion was not sufficient to promote adult regeneration.
    MeSH term(s) Animals ; Myocytes, Cardiac/metabolism ; Regeneration ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Cell Differentiation ; Mice ; Cell Proliferation ; Signal Transduction ; Myeloid Ecotropic Viral Integration Site 1 Protein/genetics ; Myeloid Ecotropic Viral Integration Site 1 Protein/metabolism ; DNA-Binding Proteins
    Chemical Substances Mbnl1 protein, mouse ; RNA-Binding Proteins ; Myeloid Ecotropic Viral Integration Site 1 Protein ; DNA-Binding Proteins
    Language English
    Publishing date 2024-03-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.123.066860
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: 1,25-Vitamin D3 promotes cardiac differentiation through modulation of the WNT signaling pathway.

    Hlaing, Su M / Garcia, Leah A / Contreras, Jaime R / Norris, Keith C / Ferrini, Monica G / Artaza, Jorge N

    Journal of molecular endocrinology

    2014  Volume 53, Issue 3, Page(s) 303–317

    Abstract: ... to induce cardiac differentiation during embryonic development and in adult cells. In conclusion ... phenotype, cell cycle progression and differentiation into cardiomyotubes. We determined that the addition ... renewal, lineage selection and, even more importantly, heart development. In this study, we examined ...

    Abstract Cardiovascular disease (CVD) remains the leading cause of death worldwide. Low levels of vitamin D are associated with high risk of myocardial infarction, even after controlling for factors associated with coronary artery disease. A growing body of evidence indicates that vitamin D plays an important role in CVD-related signaling pathways. However, little is known about the molecular mechanism by which vitamin D modulates heart development. The WNT signaling pathway plays a pivotal role in tissue development by controlling stem cell renewal, lineage selection and, even more importantly, heart development. In this study, we examined the role of 1,25-D3 (the active form of vitamin D) on cardiomyocyte proliferation, apoptosis, cell phenotype, cell cycle progression and differentiation into cardiomyotubes. We determined that the addition of 1,25-D3 to cardiomyocytes cells: i) inhibits cell proliferation without promoting apoptosis; ii) decreases expression of genes related to the regulation of the cell cycle; iii) promotes formation of cardiomyotubes; iv) induces the expression of casein kinase-1-α1, a negative regulator of the canonical WNT signaling pathway; and v) increases the expression of the noncanonical WNT11, which it has been demonstrated to induce cardiac differentiation during embryonic development and in adult cells. In conclusion, we postulate that vitamin D promotes cardiac differentiation through a negative modulation of the canonical WNT signaling pathway and by upregulating the expression of WNT11. These results indicate that vitamin D repletion to prevent and/or improve cardiovascular disorders that are linked with abnormal cardiac differentiation, such as post infarction cardiac remodeling, deserve further study.
    MeSH term(s) Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Cell Differentiation/drug effects ; Cell Nucleus/drug effects ; Cell Nucleus/metabolism ; Cells, Cultured ; Cholecalciferol/pharmacology ; Embryo, Mammalian ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/physiology ; Protein Transport/drug effects ; Rats ; Receptors, Calcitriol/metabolism ; Wnt Signaling Pathway/drug effects ; Wnt Signaling Pathway/physiology
    Chemical Substances Receptors, Calcitriol ; Cholecalciferol (1C6V77QF41)
    Language English
    Publishing date 2014-08-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 645012-x
    ISSN 1479-6813 ; 0952-5041
    ISSN (online) 1479-6813
    ISSN 0952-5041
    DOI 10.1530/JME-14-0168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Pravastatin improves function in hibernating myocardium by mobilizing CD133+ and cKit+ bone marrow progenitor cells and promoting myocytes to reenter the growth phase of the cardiac cell cycle.

    Suzuki, Gen / Iyer, Vijay / Cimato, Thomas / Canty, John M

    Circulation research

    2008  Volume 104, Issue 2, Page(s) 255–64, 10p following 264

    Abstract: ... <0.05) and the growth phase of the cell cycle (Ki67; 410+/-82 to 1261+/-235 nuclei/10(6) myocyte ... 167 cells/10(6) myocyte nuclei and cKit(+) cells from 223+/-49 to 953+/-123 cells/10(6) myocyte nuclei ... bone marrow progenitor cells and increased myocardial tissue levels (LAD CD133(+) cells from 140+/-33 to 884+ ...

    Abstract 3-hydroxy-3-methyl glutaryl coenzyme A reductase inhibitors have been reported to increase circulating bone marrow progenitor cells and variably improve global function in heart failure. The potential role of improved perfusion versus direct effects of statins on cardiac myocytes has not been established. We chronically instrumented swine with a left anterior descending artery (LAD) stenosis to produce chronic hibernating myocardium with regional contractile dysfunction in the absence of heart failure. Hemodynamics, function, perfusion, and histopathology were assessed in pigs treated for 5 weeks with pravastatin (n=12) versus untreated controls (n=10). Regional LAD wall thickening was depressed under baseline conditions (LAD 3.7+/-0.3 versus 6.6+/-0.3 in remote regions, P<0.01). It remained unchanged in untreated animals but increased from 3.8+/-0.6 to 5.2+/-0.5 mm after pravastatin (P<0.01). There was no increase in myocardial perfusion at rest or during vasodilation. Pravastatin mobilized circulating CD133(+)/cKit(+) bone marrow progenitor cells and increased myocardial tissue levels (LAD CD133(+) cells from 140+/-33 to 884+/-167 cells/10(6) myocyte nuclei and cKit(+) cells from 223+/-49 to 953+/-123 cells/10(6) myocyte nuclei). Pravastatin increased myocytes in mitosis (phospho-histone-H3; 9+/-5 to 43+/-7 nuclei/10(6) myocyte nuclei, P<0.05) and the growth phase of the cell cycle (Ki67; 410+/-82 to 1261+/-235 nuclei/10(6) myocyte nuclei, P<0.05) in diseased but not normal hearts. As a result, pravastatin increased LAD myocyte nuclear density from 830+/-41 to 1027+/-55 nuclei/mm(2) (P<0.05). These data indicate that, in the absence of impaired endothelial function and heart failure, dysfunctional hibernating myocardium improves after pravastatin. This effect is independent of myocardial perfusion and related to mobilization of CD133(+)/cKit(+) bone marrow progenitor cells which stimulate myocyte proliferation resulting in quantitative increases in myocyte nuclear density.
    MeSH term(s) AC133 Antigen ; Animals ; Antigens, CD/metabolism ; Bone Marrow Cells/drug effects ; Bone Marrow Cells/immunology ; Bone Marrow Cells/pathology ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Coronary Circulation/drug effects ; Coronary Stenosis/drug therapy ; Coronary Stenosis/pathology ; Coronary Stenosis/physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; GATA4 Transcription Factor/metabolism ; Glycoproteins/metabolism ; Hemodynamics/drug effects ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology ; Mitosis/drug effects ; Muscle Development/drug effects ; Myocardial Contraction/drug effects ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/immunology ; Myocytes, Cardiac/pathology ; Peptides/metabolism ; Pravastatin/pharmacology ; Proto-Oncogene Proteins c-kit/metabolism ; Regeneration/drug effects ; Stem Cells/drug effects ; Stem Cells/immunology ; Stem Cells/pathology ; Swine
    Chemical Substances AC133 Antigen ; Antigens, CD ; GATA4 Transcription Factor ; Glycoproteins ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Peptides ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Pravastatin (KXO2KT9N0G)
    Language English
    Publishing date 2008-12-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.108.188730
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Arresting developments in the cardiac myocyte cell cycle: role of cyclin-dependent kinase inhibitors.

    Brooks, G / Poolman, R A / Li, J M

    Cardiovascular research

    1998  Volume 39, Issue 2, Page(s) 301–311

    Abstract: ... some of our recent findings pertaining to the involvement of the cell cycle in modulating cardiac myocyte growth and ... of cardiovascular disease. In this article, we shall review the function of the cell cycle machinery and outline ... even death. Studies in proliferating cells have identified a group of genes and proteins that controls ...

    Abstract Like most other cells in the body, foetal and neonatal cardiac myocytes are able to divide and proliferate. However, the ability of these cells to undergo cell division decreases progressively during development such that adult myocytes are unable to divide. A major problem arising from this inability of adult cardiac myocytes to proliferate is that the mature heart is unable to regenerate new myocardial tissue following severe injury, e.g. infarction, which can lead to compromised cardiac pump function and even death. Studies in proliferating cells have identified a group of genes and proteins that controls cell division. These proteins include cyclins, cyclin-dependent kinases (CDKs) and CDK inhibitors (CDKIs), which interact with each other to form complexes that are essential for controlling normal cell cycle progression. A variety of other proteins, e.g. the retinoblastoma protein (pRb) and members of the E2F family of transcription factors, also can interact with, and modulate the activities of, these complexes. Despite the major role that these proteins play in other cell types, little was known until recently about their existence and activities in immature (proliferating) or mature (non-proliferating) cardiac myocytes. The reason(s) why cardiac myocytes lose their ability to divide during development remains unknown, but if strategies were developed to understand the mechanisms underlying cardiac myocyte growth, it could open up new avenues for the treatment of cardiovascular disease. In this article, we shall review the function of the cell cycle machinery and outline some of our recent findings pertaining to the involvement of the cell cycle in modulating cardiac myocyte growth and hypertrophy.
    MeSH term(s) Animals ; Cell Cycle/physiology ; Cell Cycle Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p27 ; Cyclin-Dependent Kinase Inhibitor p57 ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Cyclin-Dependent Kinases/metabolism ; Cyclins/metabolism ; Enzyme Inhibitors/metabolism ; Humans ; Hypertrophy, Left Ventricular/metabolism ; Hypertrophy, Left Ventricular/pathology ; Mammals/metabolism ; Microtubule-Associated Proteins/metabolism ; Myocardium/cytology ; Myocardium/metabolism ; Myocardium/pathology ; Nuclear Proteins/metabolism ; Tumor Suppressor Proteins
    Chemical Substances CDKN1A protein, human ; CDKN1C protein, human ; Cell Cycle Proteins ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclin-Dependent Kinase Inhibitor p57 ; Cyclins ; Enzyme Inhibitors ; Microtubule-Associated Proteins ; Nuclear Proteins ; Tumor Suppressor Proteins ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2) ; Cyclin-Dependent Kinases (EC 2.7.11.22)
    Language English
    Publishing date 1998-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1016/s0008-6363(98)00125-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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