Transcriptional activity of genes encoding Transforming Growth Factor β and its receptors in peripheral blood mononuclear cells from patients with acute coronary syndromes

Background Recent data report altered gene expression of numerous pro- and anti-inflammatory factors involved in pathology of acute coronary syndromes (ACS). Transforming growth factor β (TGFβ) signaling is engaged in a wide range of processes. Its effect on vessels seems to be protective due to its anti-inflammatory and anti-atherogenic action. However, it also seems to be engaged in such negative effects as neointima formation and fibrosis. The aim of the study was to assess the expression of the genes encoding TGFβ and its receptors (type I, II, and III) in patients with ACS. Methods The study was carried out on 24 patients with acute coronary syndrome (7 with unstable angina [UA] and 17 with myocardial infarction [MI]) and 10 age-matched healthy subjects (control). To evaluate gene expression of TGFβ and its receptors total mRNA was extracted from peripheral blood mononuclear cells (PBMC) and the number of mRNA copies were assessed by quantitative reverse transcriptase polymerase chain reaction (QRT-PCR). Results MI and UA patients demonstrated significantly lower TGFβ gene expression compared to control (2789 ± 418 c/μg vs. 20262 ± 2548 c/μg; p < 0.001, and 3390 ± 518 c/μg vs. 20262 ± 2548 c/μg; p < 0.001, respectively), as well as noticeably lower transcriptional activity of genes encoding its type I (3295 ± 447 c/μg vs. 12859 ± 1929 c/μg; p < 0.001, and 3258 ± 721 c/μg vs. 12859 ± 1929 c/μg; p < 0.01, respectively) and type II receptors (2364 ± 346 c/μg vs. 19003 ± 2357 c/μg; p < 0.001, and 2680 ± 522 c/μg vs. 19003 ± 2357 c/μg; p < 0.01, respectively). Also, gene expression of the type III receptor was inferior in the studied group compared to the control, although the difference was significant only for the UA group vs. control. Expressions of the studied genes did not differ between patients with MI and those with UA. Conclusion Our report shows that the decreased activity of TGFβ in patients with ACS is at least partly due altered transcriptional activity of genes encoding both TGFβ and its receptors, what may be responsible for the evolution of atherosclerotic lesions.