Matrix γ-Carboxyglutamic Acid Protein (MGP) G-7A and T-138C Gene Polymorphisms in Indian (Mayo and Teenek) and Mestizo Populations from Mexico

Hernández-Pacheco, Guadalupe; Murguía, Luis Enrique; Rodrı́guez-Pérez, José Manuel; Fragoso, José Manuel; Pérez-Vielma, Nadia Mabel; Martínez‐Rodríguez, Nancy; Granados, Julio; Vargas‐Alarcón, Gilberto

doi:10.1353/hub.2005.0048

Cited by 6 publications

(4 citation statements)

References 12 publications

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“…An assumed molecular mechanism of T-138C polymorphism is that it affects calcification and confers an increased risk of plaque and myocardial infarction. 25 An analysis of the MGP promoter activity revealed that the T-138C allele reduced the promoter activity by 20% in the rat vascular smooth muscle cells and by up to 50% in the human fibroblast cell line. The study also showed that a nuclear protein binds to the T-138C polymorphic site and that the binding is enhanced in the presence of the T allele.…”

Section: Discussionmentioning

confidence: 99%

No Association of Genetic Markers with Carotid Intimal Medial Thickness in β-Thalassemia Major Patients

et al. 2017

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Regular transfusion leads to cardiac siderosis resulting in cardiac complications that account for more than 71% of the total mortality in thalassemia patients. We aimed to study the variants of matrix metalloproteinase-9 (MMP9), matrix Gla protein (MGP), and estrogen receptor α(ERα), which might be contributing to atherosclerosis, leading to heart failure in thalassemia major. One hundred and five thalassemia patients on regular transfusion and iron chelation therapy were enrolled for the study. Carotid artery intimal medial thickness (CIMT) measurement was done to check for atherosclerosis. 9 (C1562T), (T138C), and α gene ( II (rs2234693T > C) and I (rs9340799A> G) polymorphism were analyzed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. CIMT values were within the normal range (<0.90 mm) in all patients. There was no difference in mean CIMT values between males and females (0.56 ± 0.11 versus 0.56 ± 0.12, = 0.928). There was no correlation of CIMT with age, body surface area, and body mass index as well as with serum ferritin levels. No statistically significant difference in frequency of MMP9, MGP, and ERα genotypes was seen in two dichotomized groups of CIMT (CIMT< 0.56 and CIMT ≥ 0.56). Variants of , , and ERα have a reserved influence on cardiac disease pathogenesis, and the disease phenotype in thalassemia patients may be more strongly impacted by other factors.

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Section: Discussionmentioning

confidence: 99%

No Association of Genetic Markers with Carotid Intimal Medial Thickness in β-Thalassemia Major Patients

et al. 2017

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“…These cells have a high potential to become mesenchymal progenitors and differentiate into osteoblasts and chondrocytes. [ 16 ] In addition, pericytes adopt a behavior similar to calcifying cells by generating in vitro calcified nodules,[ 17 ] presenting molecules such as type I collagen, OPN, matrix Gla protein (MGP),[ 18 ] and osteocalcin within the vasculature. When an atherosclerotic lesion is present, these factors act as osteoprogenitors in the vascular wall.…”

Section: P Athophysiologymentioning

confidence: 99%

Vascular Calcification

Pérez-Hernández

Aptilon-Duque

Blachman‐Braun

et al. 2017

Chinese Medical Journal

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Objective:Vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima (atherosclerotic calcification) or tunica media (Mönckenberg's sclerosis). Vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.Data Sources:We conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords “genetics and vascular calcification”, “molecular pathways, genetic and vascular calcification” and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways.Study Selection:The most valuable published original and review articles related to our objective were selected.Results:Vascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development.Conclusion:Although several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease.

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“…Серед багатьох (понад 120 варіантів) описаних однонуклеотидних поліморфізмів (SNP) у гені MGP людини найкраще досліджено три: T -138 →C (rs1800802), G -7 →A (rs1800801) та Thr 83 →Ala (rs4236) [9,10,13,18,17,23,30]. Поліморфізми T -138 →C та G -7 →A знаходяться в промоторній частині гена -ділянці, яка утворює комплекси з ядерними білками і сприймає їх регуляторні впливи.…”

Section: вступunclassified

The polymorphism of matrix Gla-protein gene in ischemic atherothrombotic stroke patients

Harbuzova¹,

Oi²,

Ataman³

et al. 2012

Fiziol Zh

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Matrix γ-Carboxyglutamic Acid Protein (MGP) G-7A and T-138C Gene Polymorphisms in Indian (Mayo and Teenek) and Mestizo Populations from Mexico

Cited by 6 publications

References 12 publications

No Association of Genetic Markers with Carotid Intimal Medial Thickness in β-Thalassemia Major Patients

No Association of Genetic Markers with Carotid Intimal Medial Thickness in β-Thalassemia Major Patients

Vascular Calcification

The polymorphism of matrix Gla-protein gene in ischemic atherothrombotic stroke patients

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