Citokine TGF-β1 - a potential diagnostic biomarker for Cardiovascular patients

Abstract

Thoracic aortic aneurysms (TAA) develop asymptomatically and cause aortic ruptures which are associated with high mortality rate. Our laboratory of Molecular Cardiology investigates mechanisms associated with TAA in order to find genetic and biochemical markers that could be implemented in hospitals for early diagnosis of TAA. A pilot study on patients with TAA (without Marfan syndrome features) focuses on interactions between Fibrillin1 (FBN1) genetic polymorphisms and levels of transforming growth factor beta 1 (TGF-β1) in patients blood plasma. Previous studies have shown that certain FBN1 polymorphisms increase the risk of developing sporadic TAA but the exact mechanism remains unclear. FBN1 and TGF-β1 interplay could be one of the major factors causing pathological defects in the thoracic aorta’s wall. We investigated FBN1 polymorphisms and TGF-β1 concentration in blood of 39 patients undergoing aortic reconstruction due to TAA and compared it to 60 healthy individuals from random population in Kaunas. TGF-β1 levels were significantly higher (p <0.05) in patients with TAA (mean 7.4) compared to healthy population (mean 4.3). TAA patients were further divided into 3 groups according to their diagnostic categories: aneurysms (21), dissections (5), and post stenotic dilatation (13). Highest levels of TGF-β1 were detected in dissections group (mean 14.5), however due to small patient number the results are not statistically reliable. Aneurysms group showed reduced levels of TGF-β1 (mean 8.3); lowest TGF-β1 concentration was observed in post stenotic dilatation group (mean 6.4). Our results show that FBN1 polymorphisms have no significant impact on TGF-β1 blood levels, thus the genetic defects in FBN1 cause TAA through a different biochemical pathway. We found increased TGF-β1 concentration in TAA patients of dissections group which could be further developed as a biochemical marker in diagnosis of TAA at [...].