Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 102, Issue 6, Pages 1375-1388Publisher
WILEY
DOI: 10.1002/jcb.21594
Keywords
endoglin; transforming growth factor-beta receptors; hereditary hemorrhagic telangiectasia; vascular pathology; vascular endothelium; vascular smooth muscle
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Funding
- NCRR NIH HHS [P20 RR015555-049001, P20 RR015555-040004, P20 RR015555, P20 RR015555-076465, RR15555] Funding Source: Medline
- NHLBI NIH HHS [R01 HL083151, R01-HL083151, R01 HL083151-01A2] Funding Source: Medline
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The broad role of the transforming growth factor beta (TGFP) signaling pathway in vascular development, homeostasis, and repair is well appreciated. Endoglin is emerging as a novel, complex, and poorly understood regulatory component of the TGFP receptor complex, whose importance is underscored by its recognition as the site of mutations causing hereditary hemorrhagic telangiectasia (HHT) [McAllister et al., 1994]. Extensive analyses of endoglin function in normal developmental mouse models [Bourdeau et al., 1999; Li et al., 1999; Arthur et al., 2000] and in HHT animal models [Bourdeau et al., 2000; Torsney et al., 20031 exemplify the importance of understanding endoglin's biochemical functions. However, novel mechanisms underlying the regulation of these pathways continue to emerge. These mechanisms include modification of TGFP receptor signaling at the ligand and receptor activation level, direct effects of endoglin on cell adhesion and migration, and emerging roles for endoglin in the determination of stem cell fate and tissue patterning. The purpose of this review is to highlight the cellular and molecular studies that underscore the central role of endoglin in vascular development and disease. J. Cell. Biochem. 102: 1375-1388, 2007. (c) 2007 Wiley-Liss, Inc.
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