Requirement of Type III TGF-β Receptor for Endocardial Cell Transformation in the Heart

Brown, Christopher B.; Boyer, Angelique; Runyan, Raymond B.; Barnett, Joey V.

doi:10.1126/science.283.5410.2080

Cited by 359 publications

(261 citation statements)

References 26 publications

(10 reference statements)

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“…This indicates that Sema6D affects the migration of both endothelial and mesenchymal cells from the CT segment and ventricle explants. This effect of Sema6D was in contrast to that of TGF-␤, which has been found to increase the mesenchymal cells from the CT segment (Brown et al 1999); TGF-␤ did not show a significant effect on the migration of endothelial cells from both explants ( Supplementary Fig. 3).…”

Section: Sema6d Displays Distinct Effects On Explants From Different mentioning

confidence: 79%

Dual roles of Sema6D in cardiac morphogenesis through region-specific association of its receptor, Plexin-A1, with off-track and vascular endothelial growth factor receptor type 2

Toyofuku¹,

Zhang²,

Kumanogoh³

et al. 2004

Genes Dev.

262

248

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Semaphorins, originally identified as axon guidance factors in the nervous system, play integral roles in organogenesis. Here, we demonstrate a critical involvement of Sema6D in cardiac morphogenesis. Ectopic expression of Sema6D or RNA interference against Sema6D induces expansion or narrowing of the ventricular chamber, respectively, during chick embryonic development. Sema6D also exerts region-specific activities on cardiac explants, a migration-promoting activity on outgrowing cells from the conotruncal segment, and a migration-inhibitory activity on those from the ventricle. Plexin-A1 mediates these activities as the major Sema6D-binding receptor. Plexin-A1 forms a receptor complex with vascular endothelial growth factor receptor type 2 in the conotruncal segment or with Off-track in the ventricle segment; these complexes are responsible for the effects of Sema6D on the respective regions. Thus, the differential association of Plexin-A1 with additional receptor components entitles Sema6D to exert distinct biological activities at adjacent regions. This is crucial for complex cardiac morphogenesis.[Keywords: Semaphorin; Plexin; cardiac development] Supplemental material is available at http://www.genesdev.org.

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Section: Sema6d Displays Distinct Effects On Explants From Different mentioning

confidence: 79%

Dual roles of Sema6D in cardiac morphogenesis through region-specific association of its receptor, Plexin-A1, with off-track and vascular endothelial growth factor receptor type 2

Toyofuku¹,

Zhang²,

Kumanogoh³

et al. 2004

Genes Dev.

262

248

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“…The function of TGFBR3 is not fully clarified; however, evidence suggests that it supports the binding of TGF-to the TGFBR1-TGFBR2 complex, albeit that it lacks a recognizable signaling domain (Lopez-Cassilas et al 1993). Experimentally induced deficiency of TGFBR3 interfered with endocardial cell transformation in the heart, supporting its essential role in TGF-signaling (Brown et al 1999). In this report, we present 12 polymorphisms and some divergences from the published sequence found by sequencing the cDNA of TGFBR3 (n ϭ 6 Caucasian individuals), based on the known sequence of a 4208-bp fragment, consisting of an open reading frame (OFR) of 2547 bp (849 amino acids), flanked by a 5Ј untranslated region (UTR) of 348 bp and a 3Ј UTR of 1310 bp (Morén et al 1992; GenBank accession no., L07594).…”

Section: Introductionmentioning

confidence: 85%

“…TGFBR3 may also facilitate TGF-binding to other receptors, stabilize multimeric receptor complexes, or segregate growth factor from activating receptors (Ji et al 1999). In testing genetic defects of the TGF-III receptor gene, the present characterization of 12 polymorphisms may be useful for further linkage or association studies on potentially related phenotypes, including developmental defects of the heart (Brown et al 1999). …”

Section: Discussionmentioning

confidence: 99%

Eleven single nucleotide polymorphisms and one triple nucleotide insertion of the human TGF-β III receptor gene

Zippert

Baßler²,

Holmer³

et al. 2000

J Hum Genet

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We found 11 single nucleotide polymorphisms and one triple nucleotide insertion in the cDNA of the human transforming growth factor (TGF-) III receptor gene (TGFBR3) located on 1p33-p32, encoding betaglycan, a component of the TGF-receptor system. Inside the 5Ј untranslated region (UTR), a GAEA polymorphism was identified at position 311. In the open reading frame (ORF), a non-conservative TAEC polymorphism was identified at position 392, and three conservative polymorphisms were found at positions 563 (GAEA), 1548 (GAEA), and 2370 (CAET). A triple nucleotide insertion (GCA) was identified at position 1419. Inside the 3Ј UTR, six polymorphisms were identified: four GAEA, at positions 2918, 3055, 3098, and 3355; one TAEA, at position 3183; and one GAEC, at position 3966. In addition to these changes, some divergences from the published sequence were observed in all 12 chromosomes tested. These included, in the ORF, an additional C after position 555, two additional G after position 563, and an additional T after position 1388. No T was found at position 1394. The alterations translate to a changed amino acid sequence. Inside the 3Ј UTR, additional discrepancies were identified. The discovered changes and polymorphisms may be useful for further genetic studies of TGFBR3 receptor deficiencies.

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“…Both G-protein-mediated (Boyer et al, 1999b, Runyan et al, 1990 and TGF␤-mediated signal transduction processes were found to direct EMT (Brown et al, 1996(Brown et al, , 1999Potts et al, 1991Potts et al, , 1992. Within the chicken system, both TGF␤2 and ␤3 isoforms are necessary for the process in separate, sequential steps (Potts and Runyan, 1989;Potts et al, 1991;Runyan et al, 1992;Boyer et al, 1999a).…”

Section: Introductionmentioning

confidence: 99%

Latrophilin‐2 is a novel component of the epithelial‐mesenchymal transition within the atrioventricular canal of the embryonic chicken heart

Doyle

Scholz

Greer

et al. 2006

Developmental Dynamics

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Endothelial cells in the atrioventricular canal of the heart undergo an epithelial-mesenchymal transition (EMT) to form heart valves. We surveyed an on-line database (http://www.geisha.arizona.edu/) for clones expressed during gastrulation to identify novel EMT components. One gene, latrophilin-2, was identified as expressed in the heart and appeared to be functional in EMT. This molecule was chosen for further examination. In situ localization showed it to be expressed in both the myocardium and endothelium. Several antisense DNA probes and an siRNA for latrophilin-2 produced a loss of EMT in collagen gel cultures. Latrophilin-2 is a putative G-protein-coupled receptor and we previously identified a pertussis toxin-sensitive G-protein signal transduction pathway. Microarray experiments were performed to examine whether these molecules were related.

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Requirement of Type III TGF-β Receptor for Endocardial Cell Transformation in the Heart

Cited by 359 publications

References 26 publications

Dual roles of Sema6D in cardiac morphogenesis through region-specific association of its receptor, Plexin-A1, with off-track and vascular endothelial growth factor receptor type 2

Dual roles of Sema6D in cardiac morphogenesis through region-specific association of its receptor, Plexin-A1, with off-track and vascular endothelial growth factor receptor type 2

Eleven single nucleotide polymorphisms and one triple nucleotide insertion of the human TGF-β III receptor gene

Latrophilin‐2 is a novel component of the epithelial‐mesenchymal transition within the atrioventricular canal of the embryonic chicken heart

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