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Vascular endothelial growth factor (VEGF) fails to improve blood flow and to promote collateralization in a diabetic mouse ischemic hindlimb model
Authors:Ariel Roguin  Samy Nitecki  Irit Rubinstein  Eviatar Nevo  Aaron Avivi  Nina S Levy  Zaid A Abassi  Edmond Sabo  Orit Lache  Meira Frank  Aaron Hoffman  Andrew P Levy
Institution:1. Department of Pharmacology and Clinical Pharmacology, University of Turku, It?inen Pitk?katu 4, FIN-20520, Turku, Finland
2. Department of Endocrinology, Malm? University Hospital, Lund University, Wallenberg Laboratory, University Hospital MAS, S-20502, Malm?, Sweden
Abstract:

Background

An insertion/deletion polymorphism in the α2B-adrenoceptor (AR) has been associated with the risk for acute myocardial infarction (AMI) and sudden cardiac death. In this study we tested whether this polymorphism is associated with the risk for AMI among members of families with type 2 diabetes.

Methods

154 subjects with a history of AMI were matched for age and sex with one of their siblings who did not have a history of AMI. The prevalence of the genotypes of the α2B-AR insertion/deletion polymorphism was compared between the siblings using McNemar's test. We also explored the data to see whether this genetic variation affects the risk for hypertension by using logistic regression models in the two subpopulations of subjects, with and without a history of AMI.

Results

Among all study subjects, 73 (24%) carried the α2B-AR deletion/deletion genotype, 103 (33%) carried the insertion/insertion genotype, and 132 (43%) were heterozygous. The distribution of genotypes of the α2B-AR insertion/deletion variation in the group of subjects with a history of AMI and their phenotype-discordant siblings did not statistically significantly differ from that expected by random distribution (p = 0.52): the deletion/deletion genotype was carried by 34 subjects with AMI (22%), and by 39 subjects without AMI (25%). Neither did we observe any significant difference in deletion allele frequencies of the α2B-AR insertion/deletion polymorphism between patients with a history of AMI (0.44) and their sib-pair controls (0.46, p = 0.65). In an exploratory analysis, the α2B-AR deletion/deletion genotype was associated with increased odds for hypertension compared with subjects carrying any of the other genotypes.

Conclusions

The deletion/deletion genotype of the α2B-AR does not emerge in this study as a risk factor for AMI among members of families with type 2 diabetes; however, it might be involved in the development of hypertension.
Keywords:
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