The Experts below are selected from a list of 288 Experts worldwide ranked by ideXlab platform
Adriana Gittenbergerde C Groot - One of the best experts on this subject based on the ideXlab platform.
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unique vascular morphology of the fourth Aortic Arches possible implications for pathogenesis of type b Aortic arch interruption and anomalous right subclavian artery
Cardiovascular Research, 1999Co-Authors: Maarten Bergwerff, Robert E. Poelmann, Marco C. Deruiter, Susan Hall, Adriana Gittenbergerde C GrootAbstract:Objective: Neural crest-derived cells were previously shown to participate in vessel wall formation of the great thoracic arteries, and their contribution was proposed to affect morphology and physiology of these vessels in the chick. The present investigation was undertaken to examine vascular differentiation and morphogenesis of the neural crest-derived Aortic Arches in mammals. Methods: Using immunohistochemical markers for smooth muscle cell differentiation and a neurofilament marker, we examined morphogenesis of the great arteries in mice, ranging from embryonic day 11.5 to the adult. Results: We observed that in the 4th Aortic arch arteries early media formation differed from the other arteries, in that they almost completely lacked (or showed decreased) actin expression in certain areas. This discontinuity in actin expression persisted throughout much of foetal development, in the form of circular segments of cells displaying decreased staining for smooth muscle markers, both at the left and right side of the arterial tree. In adult mice, the 4th arch artery derivatives, segment B of the Aortic arch and the proximal right subclavian artery, were observed to differ from adjoining vessels in their smooth muscle and elastic composition. Staining for neurofilaments revealed close association of the developing segments with apparent sensory afferent vascular innervation. Conclusion: The unique areas of the 4th arch artery identified here reflect the basic segmental patterning of the early embryonic pharyngeal Arches. These segments correlate with sites that are predisposed to interruption or severe hypoplasia, and may thus reveal part of the aetiology of type-B Aortic arch interruptions and arteria lusoria.
Lazaros Kochilas - One of the best experts on this subject based on the ideXlab platform.
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the role of neural crest during cardiac development in a mouse model of digeorge syndrome
Developmental Biology, 2002Co-Authors: Lazaros Kochilas, Sandra Merschergomez, Vijaya Potluri, Jun Liao, Raju Kucherlapati, Bernice E Morrow, Jonathan A EpsteinAbstract:The velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a genetic disorder characterized by phenotypic abnormalities of the derivatives of the pharyngeal Arches, including cardiac outflow tract defects. Neural crest cells play a major role in the development of the pharyngeal Arches, and defects in these cells are likely responsible for the syndrome. Most patients are hemizygous for a 1.5- to 3.0-Mb region of 22q11, that is suspected to be critical for normal pharyngeal arch development. Mice hemizygous for a 1.5-Mb homologous region of chromosome 16 (Lgdel/+) exhibit conotruncal cardiac defects similar to those seen in affected VCFS/DGS patients. To investigate the role of Lgdel genes in neural crest development, we fate mapped neural crest cells in Lgdel/+ mice and we performed hemizygous neural crest-specific inactivation of Lgdel. Hemizygosity of the Lgdel region does not eliminate cardiac neural crest migration to the forming Aortic Arches. However, neural crest cells do not differentiate appropriately into smooth muscle in both fourth and sixth Aortic Arches and the affected Aortic arch segments develop abnormally. Tissue-specific hemizygous inactivation of Lgdel genes in neural crest results in normal cardiovascular development. Based on our studies, we propose that Lgdel genes are required for the expression of soluble signals that regulate neural crest cell differentiation.
Maarten Bergwerff - One of the best experts on this subject based on the ideXlab platform.
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unique vascular morphology of the fourth Aortic Arches possible implications for pathogenesis of type b Aortic arch interruption and anomalous right subclavian artery
Cardiovascular Research, 1999Co-Authors: Maarten Bergwerff, Robert E. Poelmann, Marco C. Deruiter, Susan Hall, Adriana Gittenbergerde C GrootAbstract:Objective: Neural crest-derived cells were previously shown to participate in vessel wall formation of the great thoracic arteries, and their contribution was proposed to affect morphology and physiology of these vessels in the chick. The present investigation was undertaken to examine vascular differentiation and morphogenesis of the neural crest-derived Aortic Arches in mammals. Methods: Using immunohistochemical markers for smooth muscle cell differentiation and a neurofilament marker, we examined morphogenesis of the great arteries in mice, ranging from embryonic day 11.5 to the adult. Results: We observed that in the 4th Aortic arch arteries early media formation differed from the other arteries, in that they almost completely lacked (or showed decreased) actin expression in certain areas. This discontinuity in actin expression persisted throughout much of foetal development, in the form of circular segments of cells displaying decreased staining for smooth muscle markers, both at the left and right side of the arterial tree. In adult mice, the 4th arch artery derivatives, segment B of the Aortic arch and the proximal right subclavian artery, were observed to differ from adjoining vessels in their smooth muscle and elastic composition. Staining for neurofilaments revealed close association of the developing segments with apparent sensory afferent vascular innervation. Conclusion: The unique areas of the 4th arch artery identified here reflect the basic segmental patterning of the early embryonic pharyngeal Arches. These segments correlate with sites that are predisposed to interruption or severe hypoplasia, and may thus reveal part of the aetiology of type-B Aortic arch interruptions and arteria lusoria.
Jonathan A Epstein - One of the best experts on this subject based on the ideXlab platform.
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the role of neural crest during cardiac development in a mouse model of digeorge syndrome
Developmental Biology, 2002Co-Authors: Lazaros Kochilas, Sandra Merschergomez, Vijaya Potluri, Jun Liao, Raju Kucherlapati, Bernice E Morrow, Jonathan A EpsteinAbstract:The velo-cardio-facial syndrome (VCFS)/DiGeorge syndrome (DGS) is a genetic disorder characterized by phenotypic abnormalities of the derivatives of the pharyngeal Arches, including cardiac outflow tract defects. Neural crest cells play a major role in the development of the pharyngeal Arches, and defects in these cells are likely responsible for the syndrome. Most patients are hemizygous for a 1.5- to 3.0-Mb region of 22q11, that is suspected to be critical for normal pharyngeal arch development. Mice hemizygous for a 1.5-Mb homologous region of chromosome 16 (Lgdel/+) exhibit conotruncal cardiac defects similar to those seen in affected VCFS/DGS patients. To investigate the role of Lgdel genes in neural crest development, we fate mapped neural crest cells in Lgdel/+ mice and we performed hemizygous neural crest-specific inactivation of Lgdel. Hemizygosity of the Lgdel region does not eliminate cardiac neural crest migration to the forming Aortic Arches. However, neural crest cells do not differentiate appropriately into smooth muscle in both fourth and sixth Aortic Arches and the affected Aortic arch segments develop abnormally. Tissue-specific hemizygous inactivation of Lgdel genes in neural crest results in normal cardiovascular development. Based on our studies, we propose that Lgdel genes are required for the expression of soluble signals that regulate neural crest cell differentiation.
Scott E Fraser - One of the best experts on this subject based on the ideXlab platform.
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early regulative ability of the neuroepithelium to form cardiac neural crest
Developmental Biology, 2011Co-Authors: Akouavi M Ezin, John Sechrist, Marianne E Bronner, Scott E FraserAbstract:The cardiac neural crest (arising from the level of hindbrain rhombomeres 6–8) contributes to the septation of the cardiac outflow tract and the formation of Aortic Arches. Removal of this population after neural tube closure results in severe septation defects in the chick, reminiscent of human birth defects. Because neural crest cells from other axial levels have regenerative capacity, we asked whether the cardiac neural crest might also regenerate at early stages in a manner that declines with time. Accordingly, we find that ablation of presumptive cardiac crest at stage 7, as the neural folds elevate, results in reformation of migrating cardiac neural crest by stage 13. Fate mapping reveals that the new population derives largely from the neuroepithelium ventral and rostral to the ablation. The stage of ablation dictates the competence of residual tissue to regulate and regenerate, as this capacity is lost by stage 9, consistent with previous reports. These findings suggest that there is a temporal window during which the presumptive cardiac neural crest has the capacity to regulate and regenerate, but this regenerative ability is lost earlier than in other neural crest populations.