ASSOCIATION OF GENETIC POLYMORPHISMS IN
THE Matrix Gla Protein (MGP) GENE WITH CORONARY
ARTERY DISEASE AND SERUM MGP LEVELS
Karsli-Ceppioglu S1,*, Yazar S2, Keskin Y3, Karaca M4, Luleci NE3, Yurdun T1
*Corresponding Author: Seher Karsli-Ceppioglu, Ph.D., Department of Toxicology, Faculty of Pharmacy,
Marmara University, Tibbiye Street No. 49, İstanbul 34668, Turkey. Tel: +90-216-414-2962.
Fax: +90-216-345-2952. E-mail: seher.karsli@marmara.edu.tr
page: 43
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INTRODUCTION
Cardiovascular diseases (CVD) have been the main
cause of death worldwide in the past decade [1]. Efforts to
overcome these diseases have gained crucial importance
along with the increase in aging population. Screening
of traditional risk factors could not provide sufficient information
for CVD prediction. Approximately 25.0% of
patients with CVD comprise asymptomatic individuals
suffering from non fatal myocardial infarction or sudden
death [2]. Therefore, in order to elucidate the causes of
CVD, which lead to predisposition for this disease, new
risk factors assessments have to be identified.
Arterial calcification affects the endothelial layer and
the media of the vessel wall. Particularly, atherosclerotic
vascular calcification is prevalent in the aging population,
however atherosclerotic lesions can occur in earlier ages,
even during fetal life, related with parental smoking [3].
Arterial calcification was found to progress with the differentiation
of vascular smooth muscle cells (VSMCs) into
osteoblast- and chondrocyte-like cells [4]. For this reason,
the role of various bone related genes in atherosclerotic processes
were investigated to clarify underlying mechanisms
[5-7]. Matrix Gla protein (MGP), a vitamin K-dependent
matrix protein, participate in regulatory mechanisms of
vascular calcification. It is an 84-amino acid protein, mainly
expressed in bone matrix, cartilage and VSMCs.
Matrix Gla protein contains nine glutamate residues
and five of them can be γ-carboxylated by vitamin K-dependent
reaction. Gla residues have high affinity to calcium
phosphate (hydroxyapatite) compound. Knockout mouse
model experiments have demonstrated that MGP-deficient
mice exhibited abnormal and severe arterial and cartilage
calcification within a few weeks after birth [6]. Moreover,
single nucleotide polymorphisms (SNPs) of human MGP
genes lead to either reduced protein expression or loss of
function [8,9]. Previously, we investigated the associations of MGP
SNPs with cardiovascular complications in chronic kidney
disease (CKD) and end-stage renal disease [10]. We
demonstrated that rs4236 and rs12304 SNPs of the MGP
gene are significantly associated with CKD. Nonetheless,
we could not find any correlation between variation of the
MGP gene and serum MGP levels. In our present study, we
assessed the relation between rs4236 (Thr83-Ala), rs12304
(Glu60-X) and rs1800802 (T138-C) SNPs of the MGP
gene and coronary artery calcification. Furthermore, we
analyzed serum MGP levels to evaluate their correlation
with studied MGP gene variants.
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