Differential Response of Mesoderm- and Neural Crest-Derived Smooth Muscle to TGF-β1: Regulation of c-myb and α1 (I) Procollagen Genes

Gadson, Preston F.; Dalton, Michael L.; Patterson, Eugene; Svoboda, Darrell D.; Hutchinson, Leanna; Schram, David; Rosenquist, Thomas H.

doi:10.1006/excr.1996.3398

Cited by 99 publications

(76 citation statements)

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“…Previous studies have suggested that susceptibility to atherosclerosis is highly associated with cell lineage in humans and experimental animals [45][46][47] . NC-derived SMCs and mesoderm-derived SMCs are shown to be different in growth and agonist-induced gene expression patterns 48,49 . A recent report demonstrated that NC-derived SMCs were more prone to calcification than those of mesodermal origin 50 .…”

Section: Discussionmentioning

confidence: 99%

Preotic neural crest cells contribute to coronary artery smooth muscle involving endothelin signalling

et al. 2012

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Neural crest cells constitute a multipotent cell population that gives rise to diverse cell lineages. The neural crest arising from the postotic hindbrain is known as the 'cardiac' neural crest, and contributes to the great vessels and outflow tract endocardial cushions, but the neural crest contribution to structures within the heart remains largely controversial. Here we demonstrate that neural crest cells from the preotic region migrate into the heart and differentiate into coronary artery smooth muscle cells. Preotic neural crest cells preferentially distribute to the conotruncal region and interventricular septum. Ablation of the preotic neural crest causes abnormalities in coronary septal branch and orifice formation. Mice and chicks lacking endothelin signalling show similar abnormalities in the coronary artery, indicating its involvement in neural crest-dependent coronary artery formation. This is the first report that reveals the preotic neural crest contribution to heart development and smooth muscle heterogeneity within a coronary artery.

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Section: Discussionmentioning

confidence: 99%

Preotic neural crest cells contribute to coronary artery smooth muscle involving endothelin signalling

et al. 2012

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“…93 The TGF-␤ signaling pathway is selectively upregulated in the thoracic aorta; TGF-␤ induces ␣-1 procollagen production via c-myb expression in SMCs derived from the neural crest (thoracic aorta) but not from the mesoderm (abdominal aorta). 94 In addition, innervation by afferent nerves may play an important trophic role, possibly via TGF-␤ signaling, in the normal development of the aortic arch. 95 Angiotensin II, which induces TGF-␤ expression, has a marked vasoconstrictor effect on the mouse abdominal aorta but little effect on the thoracic aorta, a pattern apparently due to differences in angiotensin type 1 receptor levels.…”

Section: Tgf-␤ Pathwaysmentioning

confidence: 99%

Site Specificity of Aneurysmal Disease

2010

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“…In the vessel wall, AT1 signaling stimulates proliferation of vascular smooth muscle cells (VSMCs) and vessel wall fibrosis (22), although this may be context-dependent. In avian systems, neural crest-and mesoderm-derived VSMCs (N-and M-VSMCs, respectively) respond differently to TGF-β1, with cellular proliferation and fibrosis seen in the former and growth inhibition seen in the latter (23,24). This differential response may explain the particular predisposition of the root of the aorta-a vascular segment enriched for N-VSMCs-to undergo dilatation and dissection in MFS.…”

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confidence: 99%

Losartan, an AT1 Antagonist, Prevents Aortic Aneurysm in a Mouse Model of Marfan Syndrome

Habashi

Judge

Holm

et al. 2006

Science

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Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-β (TGF-β) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-β signaling and can be prevented by TGF-β antagonists such as TGF-β-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.MFS is a systemic disorder of connective tissue caused by mutations in FBN1, the gene encoding fibrillin-1 (1). As a principal component of the extracellular matrix microfibril (2, 3), fibrillin-1 was initially thought to play primarily a structural role in connective tissue. Several lines of evidence support an additional role as a regulator of the cytokine TGF-β (4, 5). Mice homozygous for a hypomorphic Fbn1 allele have impaired pulmonary alveolar septation associated with increased TGF-β signaling that can be prevented by perinatal administration of a polyclonal TGF-β neutralizing antibody (NAb) (5). Similarly, myxomatous

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Differential Response of Mesoderm- and Neural Crest-Derived Smooth Muscle to TGF-β1: Regulation of c-myb and α1 (I) Procollagen Genes

Cited by 99 publications

References 0 publications

Preotic neural crest cells contribute to coronary artery smooth muscle involving endothelin signalling

Preotic neural crest cells contribute to coronary artery smooth muscle involving endothelin signalling

Site Specificity of Aneurysmal Disease

Losartan, an AT1 Antagonist, Prevents Aortic Aneurysm in a Mouse Model of Marfan Syndrome

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