Early Time-Dependent Dynamic Changes of TBET and GATA3 mRNA Expressions in Patients with Acute Coronary Syndrome

Timothy H Rainer,Rebecca W Y Chan,Patrick C F Tan,Cheuk-Man Yu,Colin A Graham,Gabriel W K Yip,Cangel P Y Chan

doi:10.1155/2013/139895

Abstract

Background. T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3) play important roles in the differentiation of Th1 and Th2 subsets, which contributes to the progression of acute coronary syndrome (ACS). Objective. This study aimed to investigate the temporal change of TBET/GATA3 mRNA ratio in ACS. Methods. Thirty-three patients suspected of ACS with symptom onset within 24 hours were recruited. Blood samples were taken after arrival at the emergency department and at hourly intervals until the 6th hour. The mRNA expressions of TBET and GATA3 were quantified by a real-time RT-qPCR. Results. The TBET/GATA3 mRNA ratio was elevated dramatically in patients with acute myocardial infarction (AMI) and exhibited biphasic M-shaped release kinetics with two distinct peaks. The ratio was elevated 2 hours after symptom onset, dropped to the lowest level at 10 hours, and rose to the second peak at 14 hours. A similar biphasic M-shaped curve was observed in AMI patients with blood samples taken prior to any intervention. Conclusions. The TBET/GATA3 mRNA ratio was elevated in AMI patients throughout most of the first 20 hours after symptom onset. The biphasic M-shaped release kinetics was more likely to reflect pathophysiological changes rather than treatment effects.

Highlights

T lymphocytes differentiate into T-helper (Th) 1 and Th2 subsets, and the control of the Th1/Th2 imbalance is not fully elucidated, there is growing evidence to suggest that two transcription factors, T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3), play important roles in such differentiation [1,2,3,4]
This study aimed to investigate the temporal dynamic changes in initial mRNA expressions of TBET/GATA3 ratio in patients presenting with various clinical stages of coronary artery diseases including stable angina (SA), unstable angina (UA), and acute myocardial infarction (AMI)
The TBET/GATA3 mRNA ratios in the AMI group were significantly higher than those in the non-AMI group which included patients with SA and UA acting as the disease control group at 6 hours (1.7 versus 1.1, P = 0.007), 8 hours (1.6 versus 1.2, P = 0.006), 14 hours (2.8 versus 1.2, P = 0.035), 16 hours (2.4 versus 1.2, P = 0.020), and almost at 18 hours (1.7 versus 0.8, P = 0.060)

Summary

Introduction

T lymphocytes differentiate into T-helper (Th) 1 and Th2 subsets, and the control of the Th1/Th2 imbalance is not fully elucidated, there is growing evidence to suggest that two transcription factors, T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3), play important roles in such differentiation [1,2,3,4].Th1 is essential in the process of plaque instability and plaque rupture, which in turn are common features in the pathogenesis of acute coronary syndrome (ACS) [5,6,7]. T lymphocytes differentiate into T-helper (Th) 1 and Th2 subsets, and the control of the Th1/Th2 imbalance is not fully elucidated, there is growing evidence to suggest that two transcription factors, T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3), play important roles in such differentiation [1,2,3,4]. T-box expressed in T cells (TBET) and guanine adenine thymine adenine sequence-binding protein 3 (GATA3) play important roles in the differentiation of Th1 and Th2 subsets, which contributes to the progression of acute coronary syndrome (ACS). The TBET/GATA3 mRNA ratio was elevated dramatically in patients with acute myocardial infarction (AMI) and exhibited biphasic M-shaped release kinetics with two distinct peaks. The TBET/GATA3 mRNA ratio was elevated in AMI patients throughout most of the first 20 hours after symptom onset. The biphasic M-shaped release kinetics was more likely to reflect pathophysiological changes rather than treatment effects

Objectives

Methods

Results

Conclusion