Multiple growth factors regulate coronary embryonic vasculogenesis

Tomanek, Robert J.; Zheng, Wei; Peters, Kevin G.; Lin, Ping Chang; Holifield, Jennifer S.; Suvarna, Padma R.

doi:10.1002/dvdy.1137

Cited by 43 publications

(69 citation statements)

References 40 publications

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“…Studies have shown that VEGF mRNA is strongly expressed in the myocardium, and coronary capillary growth is dependent on VEGF during the prenatal and early postnatal period (30,31). Deficiency of VEGF 164 and VEGF 188 impairs myocardial angiogenesis and induces ischemic cardiomyopathy (5).…”

Section: Discussionmentioning

confidence: 99%

Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis

Zhao

Feng

2002

American Journal of Physiology-Heart and Circulatory Physiology

105

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We recently demonstrated that mice deficient in endothelial nitric oxide (NO) synthase (eNOS) have congenital septal defects and postnatal heart failure. However, the mechanisms by which eNOS affects heart development are not clear. We hypothesized that deficiency in eNOS impairs myocardial angiogenesis. Myocardial capillary densities were measured morphometrically in neonatal mouse hearts. In vitro tube formation on Matrigel was investigated in cardiac endothelial cells. In vivo myocardial angiogenesis was performed by implanting Matrigel in the left ventricular myocardium. Myocardial capillary densities and VEGF mRNA expression were decreased in neonatal eNOS−/− compared with neonatal wild-type mice ( P < 0.01). Furthermore, in vitro tube formation from cardiac endothelial cells and in vivo myocardial angiogenesis were attenuated in eNOS−/− compared with wild-type mice ( P < 0.01). In vitro tube formation was inhibited by N G-nitro-l-arginine methyl ester in wild-type mice and restored by a NO donor, diethylenetriamine-NO, in eNOS−/− mice ( P < 0.05). In conclusion, deficiency in eNOS decreases VEGF expression and impairs myocardial angiogenesis and capillary development. Decreased myocardial angiogenesis may contribute to cardiac abnormalities during heart development in eNOS−/− mice.

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Section: Discussionmentioning

confidence: 99%

Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis

Zhao

Feng

2002

American Journal of Physiology-Heart and Circulatory Physiology

105

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“…The epicardium and epicardially derived cells (EPDC) are pivotal to coronary vascular development (Pérez-Pomares et al, 1998;Pérez-Pomares et al, 2002;Dettman et al, 1998;Landerholm et al, 1999;Tomanek et al, 2001;Tomanek et al, 2008). However, there is not much known about the nature of the RA-dependent signals responsible for epicardial and EPDC proliferation, differentiation and involvement in myocardial growth (Kang and Sucov, 2005;Lavine et al, 2005;Merki et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Wt1 controls retinoic acid signalling in embryonic epicardium through transcriptional activation of Raldh2

et al. 2011

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SUMMARYEpicardial-derived signals are key regulators of cardiac embryonic development. An important part of these signals is known to relate to a retinoic acid (RA) receptor-dependent mechanism. RA is a potent morphogen synthesised by Raldh enzymes, Raldh2 being the predominant one in mesodermal tissues. Despite the importance of epicardial retinoid signalling in the heart, the molecular mechanisms controlling cardiac Raldh2 transcription remain unknown. In the current study, we show that Wt1-null epicardial cells display decreased expression of Raldh2 both in vivo and in vitro. Using a RA-responsive reporter, we have confirmed that Wt1-null epicardial cells actually show reduced synthesis of RA. We also demonstrate that Raldh2 is a direct transcriptional target of Wt1 in epicardial cells. A secondary objective of this study was to identify the status of RA-related receptors previously reported to be critical to epicardial biology (PDGFR,; RXR). PDGFR and PDGFR mRNA and protein levels are downregulated in the absence of Wt1, but only Pdgfra expression is rescued by the addition of RA to Wt1-null epicardial cells. RXR mRNA levels are not affected in Wt1-null epicardial cells. Taken together, our results indicate that Wt1 critically regulates epicardial RA signalling via direct activation of the Raldh2 gene, and identify a role for Wt1 in the regulation of morphogen receptors involved in the proliferation, migration, and differentiation of epicardial and epicardially-derived cells (EPDC). DEVELOPMENT 1094as previously described (Pérez-Pomares et al., 2002) using anti-PDGFR, anti-PDGFR and anti-RXR antibodies (eBioscience 14-1401-81; Sc-432; Sc-553, respectively). A non-specific rabbit IgG was used instead of the primary antibodies for negative controls. Immortalised epicardial cell lines (MEEC)Hearts from control (Wt1 GFP/+ ) and Wt1-null mice (Wt1 GFP/-) carrying the 'immorto' transgene (Jat et al., 1991) were isolated at E11.5 and cultured on 24-well gelatinised dishes containing DMEM. After 24 hours, hearts were removed and epicardial cells attached to the surface were cultured and propagated as described previously Martínez-Estrada et al. (Martínez-Estrada et al., 2010). Treatments with retinoic acid (all-trans, Sigma) were performed at 1 M concentration (24 hours). Control for the treatments was incubation with the RA vehicle (ethanol 100°, 1:1000). Western blottingWestern blots were performed as described previously (Martínez-Estrada et al., 2010). Luciferase and RA reporter assaysThe Raldh2 upstream region (830 bp) was amplified by PCR from mouse genomic DNA and cloned into the pGL4.10 vector (Promega). Primer sequences were: forward, 5Ј-AAAGCTAGCTCTCCCACGCT ATCTGG -AGT-3Ј; reverse, 5Ј-AAAAGATCTGATCTCGCTGGAAG TCATGG-3Ј. PCR product was digested with NheI and BglII and cloned into the corresponding sites upstream of the firefly luciferase construct in the pGL4.10 vector.This reporter construct (100 ng) was transfected in immortalised epicardial cells, in the presence of the indicated amounts of ...

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“…We have utilized quail heart explants in order to document the regulation of vasculogenesis and angiogenesis by specific growth factors and their interactions Tomanek, 1999, 2001;Tomanek et al, 2001Tomanek and Zheng, 2002;Holifield et al, 2004). Other studies have used chicken-quail chimeras to answer questions regarding the progenitor cells that contribute to the coronary circulation (Vrancken Peeters et al, 1997Peeters et al, , 1999Bergwerff et al, 1998;Gittenberger-de Groot et al, 1998, 2004Perez-Pomares et al, 1998;Manner, 1999;Eralp et al, 2005;Van Den Akker et al, 2005) or have examined specific aspects of coronary vessel (Bogers et al, 1989;Dettman et al, 1998;Perez-Pomares et al, 2002;Ando et al, 2004;Kattan et al, 2004;Pennisi and Mikawa, 2005).…”

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confidence: 99%

Vascular patterning of the quail coronary system during development

2006

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Recent studies have provided insights into specific events that contribute to vasculogenesis and angiogenesis in the developing coronary vasculature. This study focused on the developmental progression of coronary vascularization beginning with tube formation and ending with the establishment of a coronary arterial tree. We used electron microscopy, histology of serial sections, and immunohistochemistry in order to provide a comprehensive view of coronary vessel formation during the embryonic and fetal periods of the quail heart, a species that has been used in a number of studies addressing myocardial vascularization. Our data reveal features of progenitor cells and blood islands, tubular formation, and the anatomical relationship of a transformed periarterial tubular network and sympathetic ganglia to the emergence and branching of the right and left coronary arteries. We have traced the pattern of coronary artery branching and documented its innervation. Finally, our data include the relationship of fibronectin, laminin, and apoptosis to coronary artery growth. Our findings bring together morphological events that occur over the embryonic and fetal periods and provide a baseline for studies into the mechanisms that regulate the various events that occur during these time periods. Anat Rec Part A, 288A:989-999, 2006.2006 Wiley-Liss, Inc.

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Multiple growth factors regulate coronary embryonic vasculogenesis

Cited by 43 publications

References 40 publications

Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis

Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis

Wt1 controls retinoic acid signalling in embryonic epicardium through transcriptional activation of Raldh2

Vascular patterning of the quail coronary system during development

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