Requirement for BMP and FGF signaling during cardiogenic induction in non-precardiac mesoderm is specific, transient, and cooperative

Barron, Matthew; Gao, Ming; Lough, John

doi:10.1002/(sici)1097-0177(200006)218:2<383::aid-dvdy11>3.0.co;2-p

Cited by 147 publications

(97 citation statements)

References 47 publications

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“…This finding, which is similar to our demonstration that FGF and BMP specifically and cooperatively induce nonprecardiac mesoderm to the cardiac lineage Barron et al, 2000), caused interest in what role, if any, HAT-containing proteins such as TIP60 may have during early heart development. Accordingly, the expression pattern of chicken TIP60 (hereafter cTIP60) has been examined at the nucleic acid and protein levels during early chick embryogenesis.…”

Section: Introductionsupporting

confidence: 81%

Transient expression of TIP60 protein during early chick heart development

Lough

2002

Developmental Dynamics

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Screening of an embryonic chick cDNA library revealed a gene product termed chick TIP60 (cTIP60) due to its homology with human TIP60, a founding member of the "MYST" family of proteins that possess functional motifs, including chromo, zinc finger, and histone acetyltransferase domains. cTIP60 expression was assessed during early chick embryogenesis, at the RNA level by using reverse transcriptase-polymerase chain reaction (RT-PCR) and at the protein level by using Western blotting and immunohistochemistry. RT-PCR indicated that cTIP60 transcripts in whole embryos are present as early as Hamburger-Hamilton (HH) stage 5, diminishing after HH10. Western blotting of total embryonic protein revealed that cTIP60 was present in uniform quantities between HH3 and HH25. By contrast, Western blotting of protein from isolated hearts revealed that cTIP60 protein was strongly expressed at the earliest stages of heart development (HH11-13), diminishing thereafter. This finding was corroborated by immunohistochemistry, which revealed that cTIP60 protein was selectively expressed at high levels in the myocardium between HH 10 -14. Considered in the context of its functional domains, these findings suggest that cTIP60 modulates transcriptional processes which regulate terminal cell differentiation, proliferation, or both, during early myocardial development.

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Section: Introductionsupporting

confidence: 81%

Transient expression of TIP60 protein during early chick heart development

Lough

2002

Developmental Dynamics

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“…Upon phosphorylation, these receptor-regulated (R)-Smads form complexes with Smad4, which are subsequently translocated to the nucleus to regulate activation of transcription factors, such as cardiac transcription factors Nkx-2.5, GATA-4, and Tbx factors (Massague and Chen 2000;Schlange, Andree et al 2000;Moustakas, Souchelnytskyi et al 2001;Attisano and Wrana 2002;Harvey 2002;Wakefield and Roberts 2002;Attisano and Labbe 2004;. FGF family proteins (FGF-2 and FGF-4) have been shown to support cardiomyocyte induction during embryonic development mainly by stimulating proliferation of mesodermal cells in vitro (Mima, Ueno et al 1995;Lough, Barron et al 1996;Schultheiss and Lassar 1997;Ladd, Yatskievych et al 1998;Barron, Gao et al 2000;Kawai, Takahashi et al 2004). During embryogenesis, these growth factors, originating from the anterior and lateral endoderm, synergize in a precise spatial and temporal program to support and induce cardiogenesis in neighboring precardiac mesoderm (Figure 1.2).…”

Section: Inductive Signals From the Anteriolateral(embryogenesis)/primentioning

confidence: 99%

“…TGF-β1 and activin appear to have a similar effect in inducing cardiomyocyte differentiation in posterior epiblast tissue (including regions not fated to form heart) (Yatskievych, Ladd et al 1997;Ladd, Yatskievych et al 1998), but not in non-cardiogenic mesoderm (Schultheiss, Burch et al 1997;Ladd, Yatskievych et al 1998). Conversely, BMP-2 and -4, in combination with FGF-4, induce cardiac differentiation of non-cardiogenic mesoderm (Lough, Barron et al 1996;Schultheiss and Lassar 1997;Ladd, Yatskievych et al 1998;Barron, Gao et al 2000), but fail to support cardiogenesis in posterior epiblast. FGF-2 is expressed in both endoderm as well as myocardial cells of the developing embryo (Parlow, Bolender et al 1991;Sugi, Sasse et al 1993).…”

Section: Inductive Signals From the Anteriolateral(embryogenesis)/primentioning

confidence: 99%

Geometric Control of Cardiomyogenic Induction in Human Pluripotent Stem Cells

Bauwens

Song

Thavandiran

et al. 2011

Tissue Engineering Part A

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Pluripotent stem cells provide the opportunity to study human cardiogenesis in vitro, and are a renewable source of tissue for drug testing and disease models, including replacement cardiomyocytes that may be a useful treatment for heart failure. Typically, differentiation is initiated by forming spherical cell aggregates wherein an extraembryonic endoderm (ExE) layer develops on the surface. Given that interactions between endoderm and mesoderm influence embryonic cardiogenesis, we examined the impact of human embryonic stem cell (hESC) aggregate size on endoderm and cardiac development. We first demonstrated aggregate size control by micropatterning hESC colonies at defined diameters and transferring the colonies to suspension. The ratio of endoderm (GATA-6) to neural (PAX6) gene and protein expression increased with decreasing colony size. Subsequently, maximum mesoderm and cardiac induction occurred in larger aggregates when initiated with endoderm-biased hESCs (high GATA-6:PAX6), and in smaller aggregates when initiated with neural-biased hESCs (low GATA-6:PAX6). Additionally, incorporating micropatterned aggregates in a stirred suspension bioreactor increased cell yields and contracting aggregate frequency. We next interrogated the relationship between aggregate size and endoderm and cardiac differentiation efficiency in sizecontrolled aggregates, generated using forced aggregation, in defined cardiogenic medium.

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“…After Cu treatment for 24 h, cells were fixed in 4% paraformaldehyde in PBS. After fixation, the culture chamber was incubated with monoclonal anti-α-sarcomeric-actin antibody (Sigma-Aldrich) followed by incubation with FITC-conjugated goat anti-mouse IgM [12]. Fluorescence was visualized by a phase contrast microscope (Nikon Instruments, Melville, NY).…”

Section: Immunocytochemistrymentioning

confidence: 99%

Copper reverses cardiomyocyte hypertrophy through vascular endothelial growth factor-mediated reduction in the cell size

Zhou

Jiang

Kang

2008

Journal of Molecular and Cellular Cardiology

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Previous studies have shown that dietary copper supplementation reversed heart hypertrophy induced by pressure overload in a mouse model. The present study was undertaken to understand the cellular basis of copper-induced regression of cardiac hypertrophy. Primary cultures of neonatal rat cardiomyocytes were treated with phenylephrine at a final concentration of 100 μM in cultures for 48 h to induce cellular hypertrophy. The hypertrophied cardiomyocytes were exposed to copper sulfate at a final concentration of 5 μM in cultures for additional 24 h. This copper treatment reduced the size of the hypertrophied cardiomyocytes, as measured by flow cytometry, protein content in cells, cell volume and cardiomyocyte hypertrophy markers including beta myosin heavy chain protein, skeletal alpha-actin, and atrial natriuretic peptide. Cell cycle analysis and cell sorting of p-histone-3 labeled cardiomyocytes indicated that cell division was not involved in the copper-induced regression of cardiomyocyte hypertrophy. Copper also inhibited PE-induced apoptosis, determined by a TUNEL assay. Because copper stimulates vascular endothelial growth factor (VEGF) production through activation of hypoxia-inducible transcription factor, an anti-VEGF antibody at a final concentration of 2 ng/ml in cultures was used and shown to blunt copper-induced regression of cell hypertrophy. Conversely, VEGF alone at a final concentration of 0.2 μg/ml reversed cell hypertrophy as the same as copper did. This study demonstrates that both copper and VEGF reduce the size of hypertrophied cardiomyocytes, and copper regression of cardiac hypertrophy is VEGF dependent.

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Requirement for BMP and FGF signaling during cardiogenic induction in non-precardiac mesoderm is specific, transient, and cooperative

Cited by 147 publications

References 47 publications

Transient expression of TIP60 protein during early chick heart development

Transient expression of TIP60 protein during early chick heart development

Geometric Control of Cardiomyogenic Induction in Human Pluripotent Stem Cells

Copper reverses cardiomyocyte hypertrophy through vascular endothelial growth factor-mediated reduction in the cell size

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