To evaluate the expression of atherosclerosis-associated genes in patients with hypertension and type 2 diabetes mellitus.
Twenty-seven patients (14 men, 13 women), mean age 43.26 ± 11.69 years, were included in the study, which was divided into three groups: group 1 – patients with newly diagnosed hypertension and normal glucose tolerance (n = 9), group 2 – normotensive individuals with newly diagnosed type 2 diabetes (n = 9), and control group – normotensive individuals with normal glucose tolerance (n = 9). Gene expression analysis was performed with Human Atherosclerosis RT2 Profiler PCR Array.
In patients with hypertension, we found eight genes with increased expression – FABP3, FAS, FN1, IL1R2, LPL, SERPINE1, TGFB1, and VCAM1. Decreased expression was observed for two genes – SELPLG and SERPINEB2. In patients with type 2 diabetes we found seven up-regulated genes – APOE, BAX, MMP1, NFKB1, PDGFB, SPP1, and TGFB2, whereas no specifically down-regulated genes were observed. Three genes – KLF2, PDGFRB, and PPARD were found to be expressed only in groups 1 and 2.
Hypertension is associated with increased expression of FABP3, FAS, FN1, IL1R2, LPL, SERPINE1, TGFB1, and VCAM1 and decreased expression of SELPLG and SERPINEB2. The up-regulation of FAS, FN1, SERPINE1, TGFB1, and VCAM1 might be associated with an increased cardiovascular risk. Type 2 diabetes is associated with increased expression of APOE, BAX, MMP1, NFKB1, PDGFB, SPP1, and TGFB2. KLF2 and PPARD might be part of protective mechanisms that limit target organ damage in both disease conditions. Expression of PDGFRB might play an important role in the pathogenesis of both hypertension and type 2 diabetes.
aDepartment of Diabetology, Clinical Center of Endocrinology
bDepartment of Medical Genetics
cDepartment of Physiology, Medical University Sofia, Bulgaria
Correspondence to Nikolay Stoynev, MD, Department of Diabetology, Clinical Center of Endocrinology, 2 Zdrave Str., Sofia 1431, BulgariaTel: +359 2 895 6204; e-mail: email@example.com
Received 9 July, 2012
Revised 11 September, 2012
Accepted 7 December, 2012