Transforming growth factor-beta1 in heart development

Engelmann, Gary L.; Boehm, Keith D.; Birchenall-Roberts, Maria C.; Ruscetti, Francis W.

doi:10.1016/0925-4773(92)90001-z

Cited by 43 publications

(18 citation statements)

References 52 publications

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“…Most of the reported approaches involve autologous bone marrow stem cells or myoblasts, but these cells have limited plasticity and impaired viability of the transferred cells in the area of ischemic lesion [7]. Moreover, the complex cell by microenvironment interactions, which are criti- A major determinant of engraftment and host organ-specific differentiation of donor primordial cells is the array of growth factors that are known to promote cardiogenesis and proliferation and to prevent apoptosis and cell death [8][9]. A distinct role is displayed by insulin-like growth factor-1 (IGF-1); it promotes cell mitogenesis and proliferation in early developmental stages and causes eccentric myocardial hypertrophy in the adult.…”

Section: Introductionmentioning

confidence: 99%

Insulin‐Like Growth Factor Promotes Engraftment, Differentiation, and Functional Improvement after Transfer of Embryonic Stem Cells for Myocardial Restoration

Kofidis¹,

Bruin²,

Yamane

et al. 2004

STEM CELLS

123

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Insulin-like growth factor-1 (IGF-1) promotes myocyte proliferation and can reverse cardiac abnormalities when it is administered in the early fetal stage. Supplementation of a mouse embryonic stem cell (ESC) suspension with IGF-1 might enhance cellular engraftment and host organ-specific differentiation after injection in the area of acute myocardial injury. In the study reported here, we sought to enhance the restorative effect of ESCs in the injured heart by adding IGF-1 to the injected cell population. Green fluorescent protein (GFP)-labeled sv129 ESCs (2.5 ✕ 10 5 ) were injected into the ischemic area after left anterior descending (LAD) artery ligation in BalbC mice. Recombinant mouse IGF-1 (25 ng) was added to the cell suspension prior to the injection (n = 5).

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Section: Introductionmentioning

confidence: 99%

Insulin‐Like Growth Factor Promotes Engraftment, Differentiation, and Functional Improvement after Transfer of Embryonic Stem Cells for Myocardial Restoration

Kofidis¹,

Bruin²,

Yamane

et al. 2004

STEM CELLS

123

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“…11 Members of the transforming growth factor-␤ 1 (TGF-␤) superfamily, namely, TGF-␤ and bone morphogenic protein-2, applied to undifferentiated murine ESC, upregulated mRNA of mesodermal and cardiac-specific transcription factors. 12 Embryoid bodies generated from stem cells primed with these growth factors demonstrated an increased potential for cardiac differentiation with a significantly higher occurrence of beating areas and enhanced myofibrillogenesis. 13 Fibroblast growth factor (FGF) has been linked to the expression of intermediate filaments and desmin in the cytoplasmic and cytoskeletal compartments, suggesting that FGF plays a role in cardiomyocyte differentiation during the early stages of development.…”

mentioning

confidence: 99%

Stimulation of Paracrine Pathways With Growth Factors Enhances Embryonic Stem Cell Engraftment and Host-Specific Differentiation in the Heart After Ischemic Myocardial Injury

et al. 2005

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Background-Growth factors play an essential role in organogenesis. We examine the potential of growth factors to enhance cell engraftment and differentiation and to promote functional improvement after transfer of undifferentiated embryonic stem cells into the injured heart. Methods and Results-Green fluorescent protein (GFP)-positive embryonic stem cells derived from 129sv mice were injected into the ischemic area after left anterior descending artery ligation in allogenic (BALB/c) mice. Fifty nanograms of recombinant mouse vascular endothelial growth factor, fibroblast growth factor (FGF), and transforming growth factor (TGF) was added to the cell suspension. Separate control groups were formed in which only the growth factors were given. Echocardiography was performed 2 weeks later to evaluate heart function (fractional shortening [FS]), end-diastolic diameter, and left ventricular wall thickness). Hearts were harvested for histology (connexin 43, ␣-sarcomeric actin, CD3, CD11c, major histocompatability complex class I, hematoxylin-eosin). Degree of restoration (GFP-positive graft/infarct area ratio), expression of cardiac markers, host response, and tumorigenicity were evaluated.

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“…Neonatal growth of the rodent heart involves three phases. 33 - 34 During fetal and early neonatal periods (birth to 4 days postpartum), the heart enlarges as a result of cardiomyocyte hyperplasia. Approximately 6 to 14 days postpartum, a transition from hyperplastic to hypertrophic growth occurs, resulting from karyokinesis without cytokinesis.…”

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confidence: 99%

“…34 Furthermore, in primary fetal and neonatal cardiomyocyte cultures, TGF-/31 inhibits mitogen-stimulated DNA synthesis. 34 Thus, TGF-/31 may function to regulate neonatal heart growth and development by modulating cardiomyocyte proliferation and differentiation.…”

mentioning

confidence: 99%

“…Expression of members of the actin and myosin gene families in TGF-j31-deficient animals is currently being examined because treatment of primary cultures of cardiac myocytes with TGF-/31 has been reported to elicit expression of fetal contractile protein isoforms. 41 In addition, the potential role of TGF-01 in modulating postnatal transition from hyperplastic to hypertrophic heart growth 34 suggests that a detailed examination of heart development in homozygous mutant animals may reveal cardiac abnormalities resulting from perturbations in the transition from hyperplastic to hypertrophic growth. Quantitative analyses of cell densities of cardiomyocytes and nonmuscle cells in hearts from wild-type and TGF-/31-deficient mice will be determined to address this question.…”

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confidence: 99%

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Embryonic stem cell model systems for vascular morphogenesis and cardiac disorders.

et al. 1993

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To better understand the formation of the cardiovascular system and its disease states, models amenable to manipulation must be developed. In this article we present two models. One is a small animal model for an inflammatory disorder that can lead to heart failure. Production of this model is based on the ability of blastocyst-dertved embryonic stem cells, which can be genetically altered in vitro by a technique called gene targeting, to reconstitute an entire animal when reintroduced into a blastocyst and allowed to colonize the germ line of the resulting chimeric embryo. The other model is based on the capacity of embryonic stem cells to differentiate in culture into embryo-like structures called embryoid bodies. Embryoid bodies contain angioblasts, or prevascular endothelial cells, which can be induced to undergo aspects of vascular development by manipulation of culture conditions. unique opportunities to develop model systems for poorly understood developmental processes and human diseases. The embryonic stem (ES) cell is one of the vehicles by which these models are generated. ES cells are established as a cell line from the inner cell mass cells of a mouse blastocyst. These cells are naturally immortal and can be cultured and repeatedly frozen and thawed without losing their stem cell characteristics.

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Transforming growth factor-beta1 in heart development

Cited by 43 publications

References 52 publications

Insulin‐Like Growth Factor Promotes Engraftment, Differentiation, and Functional Improvement after Transfer of Embryonic Stem Cells for Myocardial Restoration

Insulin‐Like Growth Factor Promotes Engraftment, Differentiation, and Functional Improvement after Transfer of Embryonic Stem Cells for Myocardial Restoration

Stimulation of Paracrine Pathways With Growth Factors Enhances Embryonic Stem Cell Engraftment and Host-Specific Differentiation in the Heart After Ischemic Myocardial Injury

Embryonic stem cell model systems for vascular morphogenesis and cardiac disorders.

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