左主干暨冠状动脉分叉病变峰会，CBS2019 - CBS 2019

急性冠脉综合征

OPTIMAL USE OF LIPID-LOWERING THERAPY AFTER ACUTE CORONARY SYNDROMES: A Position Paper endorsed by the International Lipid Expert Panel (ILEP) Stent Thrombosis Risk Over Time on the Basis of Clinical Presentation and Platelet Reactivity: Analysis From ADAPT-DES Effect of Lipoprotein (a) Levels on Long-term Cardiovascular Outcomes in Patients with Myocardial Infarction with Nonobstructive Coronary Arteries Percutaneous Coronary Intervention for Chronic Total Occlusion—The Michigan Experience: Insights From the BMC2 Registry 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC) Optimal medical therapy vs. coronary revascularization for patients presenting with chronic total occlusion: A meta-analysis of randomized controlled trials and propensity score adjusted studies Inflammatory Bowel Disease and Acute Coronary Syndromes: From Pathogenesis to the Fine Line Between Bleeding and Ischemic Risk Antithrombotic Therapy in Patients With Atrial Fibrillation and Acute Coronary Syndrome

Sort by hits |<<... 16 17 18 19 20 21 22 ...>>|

Original ResearchVolume 72, Issue 8, August 2018

JOURNAL： Article Link

Deficiency of GATA3-Positive Macrophages Improves Cardiac Function Following Myocardial Infarction or Pressure Overload Hypertrophy

MJ Yang, L Song, L Wang et al. Keywords: cardiac hypertrophy; inflammation; macrophage transcription factor

ABSTRACT

BACKGROUND - Macrophages are highly plastic cells that play an important role in the pathogenesis of cardiovascular disease.

OBJECTIVES - This study investigated the role of GATA3-positive macrophages in modulating cardiac function after myocardial infarction (MI) or in response to pressure overload hypertrophy.

METHODS - Myeloid-specific GATA3-deficient (mGATA3KO) mice were generated, MI or pressure overload was induced, and cardiac function was determined by echocardiography. GATA3-sufficient Cre mice were used as a control. Immunohistochemical staining, flow cytometry, MILLIPLEX Mouse Cytokine/Chemokine Assay, cultured macrophages, quantitative real-time polymerase chain reaction, and western blot were used to determine the role of GATA3 in macrophages.

RESULTS - GATA3-positive macrophages rapidly accumulated in the infarcted region of the myocardium after acute MI. Deficiency of GATA3-positive macrophages led to a significant improvement of cardiac function in response to acute MI or pressure overload hypertrophy compared with the control mice. This improvement was associated with the presence of a large number of proinflammatory Ly6Chi monocytes/macrophages and fewer reparative Ly6Clomacrophages in the myocardium of mGATA3KO mice compared with control mice. Analysis of serum proteins from the 2 mouse genotypes revealed no major changes in the profile of serum growth factors and cytokines between the 2 mice genotypes before and after MI. GATA3 was found to be specifically and transiently induced by interleukin 4 in cultured macrophages through activity of the proximal promoter, whereas the distal promoter remained silent. In addition, the absence of GATA3 in macrophages markedly attenuated arginase-1 expression in cultured macrophages.

CONCLUSIONS - We demonstrated that the presence of GATA3-positive macrophages adversely affects remodeling of the myocardium in response to ischemia or pressure overload, whereas the absence of these macrophages led to a significant improvement in cardiac function. Targeting of signaling pathways that lead to the expression of GATA3 in macrophages may have favorable cardiac outcomes.

Abstract

Recommended Article

Deficiency of GATA3-Positive Macrophages Improves Cardiac Function Following Myocardial Infarction or Pressure Overload Hypertrophy

ABSTRACT