A common polymorphism of the transforming growth factor-beta1 gene and coronary artery disease.
نویسندگان
چکیده
Transforming growth factor-β1 (TGF-β1) is a multifunctional cytokine involved in many physiological and pathological processes. Its actions are complex and in vitro experiments and clinical findings suggest that under different circumstances it may have opposing biological effects [1]. There are in vitro experimental data indicating that it may be both anti-atherogenic [2] and proatherogenic [3]. With regard to clinical studies, Grainger et al. [4] reported that serum active TGF-β1 levels were depressed in 31 patients with triple-vessel coronary disease, whereas we showed that levels were higher in patients with triple vessel disease (n ̄ 72) than in those with two vessel one vessel disease or in normal coronary arteries (n ̄ 197) [5]. These contradictory observations could result from a real difference in biological effects at different stages of the disease or be an artifact, perhaps related to a difference in the sample sizes of the two studies. Also, there is a high intra-individual variation in active TGF-β1 levels and a single active TGF-β1 measurement may not provide a reliable estimate of the true TGF-β1 status. This could be particularly relevant to atherogenesis – a chronic process occurring over decades. However, DNA variants at the TGF-β1 gene, if functional or in linkage with functional changes, could be reliable markers for TGF-β1 action and reflect a true estimate of its relationship with atherogenesis. Since TGF-β1 is a highly conserved protein, mutations at coding regions, if functional, are likely to be fatal. Common variants at non-coding regions, particularly the promoter region on the other hand, could have quantitative but non-fatal effects. Such DNA variants could be particularly relevant to genetically determined susceptibility to common diseases such as coronary artery disease (CAD). Recently, Cambien et al. [6] identified a number of DNA variants at the TGF-β1 locus in both the
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عنوان ژورنال:
- Clinical science
دوره 95 6 شماره
صفحات -
تاریخ انتشار 1998