Thrombospondin-4-Ala387Pro polymorphism is not associated with vascular function and risk of coronary heart disease in US men and women [4]

Thrombosis and Haemostasis (Impact Factor: 4.98). 04/2006; 95(3):589-90. DOI: 10.1267/THRO06030589
Source: PubMed
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    ABSTRACT: The thrombospondins are a 5-member gene family that mediate cell-cell and cell-matrix interactions. The thrombospondins are either trimers or pentamers, and their functions depend on their abilities to interact with numerous extracellular ligands and cell surface receptors through the multiple domains that compose each subunit. Recent genetic studies have indicated associations of particular single nucleotide polymorphisms in 3 of the 5 thrombospondins with cardiovascular disease. This observation has stimulated efforts to understand how the thrombospondins influence cardiovascular pathology, to dissect how the individual polymorphisms alter the structure and function of the parent thrombospondin molecules, and to replicate the genetic data in different patient populations. This review seeks to summarize current information that has emerged on each of these fronts.
    Arteriosclerosis Thrombosis and Vascular Biology 10/2007; 27(9):1886-94. DOI:10.1161/ATVBAHA.107.141713 · 6.00 Impact Factor
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    ABSTRACT: In addition to its major structural elements, extracellular matrix contains a number of factors that are important for orchestrating developmental morphogenesis, maintaining tissue homeostasis in adults, and regenerating tissue following injury. Several proteins that serve these functions share a complex modular structure that enables them to interact with specific components of the matrix while engaging specific cell surface receptors through which they control cell behavior. These have been named matricellular proteins. Matricellular proteins, including the thrombospondins, some thrombospondin-repeat superfamily members, tenascins, SPARC, CCN proteins, and SIBLING proteins, are increasingly recognized to play important roles in inherited disorders, responses to injury and stress, and the pathogenesis of several chronic diseases of aging. Improved understanding of the functions and mechanisms of action of matricellular proteins is beginning to yield novel therapeutic strategies for prevention or treatment of these diseases.
    02/2011: pages 369-413;
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    ABSTRACT: This study aimed to assess the association between single nucleotide polymorphisms in thrombospondin-1 (THBS1), thrombospondin-2 (THBS2), thrombospondin-4 (THBS4) and coronary artery disease (CAD) risk. Electronic databases were searched before June, 2014 to obtain articles associated with thrombospondin polymorphisms and CAD risk. After identifying case-control studies, odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to pool effect sizes. Different effect models were used according to heterogeneity. Meta-regression and sensitivity analyses were performed to examine the heterogeneity source. Begg's funnel plot and Egger's test were conducted for publication bias. 13 studies involving 10,801 cases and 9,381 controls were included. Associations were observed between the THBS1 N700S polymorphism and CAD risk in general population(heterozygote model: OR=1.14, 95% CI: 1.03-1.26; dominant model: OR=1.13, 95% CI: 1.00-1.29), European population (heterozygote model: OR=1.13, 95% CI: 1.00-1.27) and Asian population (heterozygote model: OR=1.57, 95% CI: 1.01-2.44; dominant model: OR=1.56, 95% CI: 1.00-2.43). The THBS2 3' untranslated region (UTR) polymorphism and THBS4 A387P polymorphism were not associated with overall CAD risk. However, an association was observed between the THBS4 A387P polymorphism and CAD risk in the American population (allele model: OR=1.09, 95% CI: 1.00-1.18; homozygote model: OR=1.29, 95% CI: 1.04-1.61; recessive model: OR=1.27, 95% CI: 1.02-1.58). The THBS1 N700S polymorphism was associated with increased CAD risk, especially in Asian and European populations. No association was observed between the THBS2 3' UTR polymorphism and CAD risk. The THBS4 A387P polymorphism was associated with increased CAD risk in the American population. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Thrombosis Research 04/2015; 136(1). DOI:10.1016/j.thromres.2015.04.019 · 2.45 Impact Factor