Please use this identifier to cite or link to this item: http://hdl.handle.net/10201/49414

Title: Controlling angiogenesis by two unique TGF-β type I receptor signaling pathways
Issue Date: 2011
Publisher: F. Hernández y J.F. Madrid. Murcia: Universidad de Murcia, Departamento de Biología Celular e Histología.
ISSN: 1699-5848
0213-3911
Related subjects: 61 - Medicina
Keywords: Angiogenesis
Pulmonary arterial hypertension
Abstract: Genetic studies in mice and humans have revealed a pivotal function for transforming growth factor-beta (TGF-β) in vascular development and maintenance of vascular homeostasis. Mice deficient for various TGF-β signaling components develop an embryonic lethality due to vascular defects. In patients, mutations in TGF-β receptors have been linked to vascular dysplasia like Hereditary Hemorrhagic Telangiectasia (HHT) and pulmonary arterial hypertension (PAH). Besides indirect effects by regulating the expression of angiogenic regulators, TGF-β also has potent direct effects on endothelial cell growth and migration, and we have proposed that TGF-β regulates the activation state of the endothelium via two opposing type I receptor/Smad pathways, activin receptor-like kinase (ALK)1 and ALK5. TGF-β is also critical for the differentiation of mural precursors into pericytes and smooth muscle cells. Furthermore, defective paracrine TGF-β signaling between endothelial and neighboring mural cells may be responsible for a leaky vessel phenotype that is characteristic of HHT. In this review, we discuss our current understanding of the TGF-β signaling pathway and its regulation of endothelial and vascular smooth muscle cell function.
Primary author: Orlova, Valeria V.
Liu, Zhen
Goumans, Marie-José
ten Dijke, Peter
Published in: Histology and histopathology, Vol. 26, nº9 (2011)
URI: http://hdl.handle.net/10201/49414
Document type: info:eu-repo/semantics/article
Number of pages / Extensions: 12
Rights: info:eu-repo/semantics/openAccess
Appears in Collections:Vol.26, nº9 (2011)

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