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Nanjing Heart Center
Asian Bifurcation Club (ABC)
Nanjing First Hospital, Nanjing Medical University
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Chinese Society of Cardiology (CSC)
Capacity Building and Continuing Education Center,National Health and Family Planning Commission (CBCEC)
American Society for Cardiovascular Angiography and Interventions (SCAI)
Asian Heart Society (AHS)
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Hongjuan Peng :
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Haimei Xu +86-13914736846
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Ling Lin : +86 (25) 52271398
+86-13951884596
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Yingying Zhao :+86-13815408517
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Recommended Paper
Management of Acute Myocardial Infarction During the COVID-19 Pandemic
COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up
CSC Expert Consensus on Principles of Clinical Management of Patients with Severe Emergent Cardiovascular Diseases during the COVID-19 Epidemic
ACC Clinical Bulletin Focuses on Cardiac Implications of Coronavirus (COVID-19)
急性冠脉综合征
Original ResearchVolume 72, Issue 8, August 2018
JOURNAL： Article Link
MJ Yang, L Song, L Wang et al. Keywords: cardiac hypertrophy; inflammation; macrophage transcription factor
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.
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