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

Yang, Mingjie; Song, Lei; Wang, Lai; Yukht, Ada; Ruther, Haley; Li, Fuqiang; Qin, Minghui; Ghiasi, Homayon; Sharifi, Behrooz G.; Shah, Prediman K.

doi:10.1016/j.jacc.2018.05.061

Cited by 51 publications

(50 citation statements)

References 72 publications

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Section: Plos Pathogensmentioning

confidence: 99%

“…Effect of M2 macrophages on HSV-1 infection M2 polarization of macrophages in the HSV-1 ocular infection, we used myeloid-specific GATA3-defieicnt mice (designated as M2 -/mice hereafter) [29]. We have previously reported that the cardiac function is significantly improved in M2 -/mice compared with the WT in response to ischemic injury [29]. We have shown that this improvement was associated with the presence of large number of pro-inflammatory Ly6C hi monocytes/macrophages and few Ly6C lo reparative macrophages in the infracted myocardium of M2 -/mice compared with the WT mice.…”

Section: Plos Pathogensmentioning

confidence: 99%

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Increased phagocytosis in the presence of enhanced M2-like macrophage responses correlates with increased primary and latent HSV-1 infection

et al. 2020

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After HSV-1 infection, macrophages infiltrate early into the cornea, where they play an important role in HSV-1 infection. Macrophages are divided into M1 or M2 groups based on their activation. M1 macrophages are pro-inflammatory, while M2 macrophages are antiinflammatory. Macrophage phenotypes can shift between M1 or M2 in vitro and in vivo following treatment with specific cytokines. In this study we looked at the effect of M2 macrophages on HSV-1 infectivity using mice either lacking M2 (M2-/-) or overexpressing M2 (M2-OE) macrophages. While presence or absence of M2 macrophages had no effect on eye disease, we found that over expression of M2 macrophages was associated with increased phagocytosis, increased primary virus replication, increased latency, and increased expression of pro-and anti-inflammatory cytokines. In contrast, in mice lacking M2 macrophages following infection phagocytosis, replication, latency, and cytokine expression were similar to wild type mice. Our results suggest that enhanced M2 responses lead to higher phagocytosis, which affected both primary and latent infection but not reactivation.

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Section: Plos Pathogensmentioning

confidence: 99%

Section: Plos Pathogensmentioning

confidence: 99%

Increased phagocytosis in the presence of enhanced M2-like macrophage responses correlates with increased primary and latent HSV-1 infection

et al. 2020

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“…In study of Pors et al, GATA3 showed obvious role in identifying mesonephric and mesonephric-like carcinomas of the gynecologic tract [40]. However, Yang et al indicated that deficiency of GATA3-positive macrophages improves cardiac function in the patients with myocardial infarction or pressure overload hypertrophy [41]. Since the function of GATA3 and its relationship with miR-374b was vague, it deserved to be further investigated.…”

Section: Discussionmentioning

confidence: 99%

MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B

Gao¹,

Bai²,

Wang³

et al. 2019

neo

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In the present study, a series of experiments were conducted to explore the function of miR-374b and the regulatory relationship among miR-374b, GATA3 and SEMA3B in glioma. MiR-374b mimics and inhibitors were employed to regulate miR-374b expression. Besides, qRT-PCR assay was used for detecting the expression level of miR-374b, GATA3 and SEMA3B mRNAs. To verify the targeting relationship between miR-374b and GATA3, dual luciferase analysis was utilized. Moreover, chromatin immunoprecipitation (ChIP) assay was performed to identify the correlation GATA3 with SEMA3B. Furthermore, si1-GATA3, si2-GATA3 and pc-GATA3 were used to regulate GATA3 expression and pc-SEMA3B served for dysregulation the SEMA3B. For assessing the significance of miR374b alone or in cooperation with GATA3 or SEMA3B on cell viability, migration and apoptosis, CCK-8, transwell and FCM assay were also performed. We found that overexpression of miR-374b, which was identified in glioma tissues and cell lines (U251, LN-299 and GOS-3) promoted cell migration and enhanced cell viability but inhibited apoptosis in this study. Furthermore, GATA3 contributed to increase the cell viability and migration and decrease the apoptosis targeted by miR-374b as evidenced by dual luciferase assay. Moreover, GATA3 binding to the promoter of SEMA3B, involved in regulating SEMA3B, was revealed. Further, a series of studies demonstrated that miR-374b targeted GATA3 regulating SEMA3B and resulted in elevation of cell viability and migration but suppressed the apoptosis. However, the promotion effects of miR-374 in glioma process were reversed by co-transfecting pc-GATA3 or pc-SEMA3B. In conclusion, miR-374b promotes glioma process in vitro through suppressing SEMA3B via targeting GATA3. The result of this study provides an important clue to the optimal treatment schedule for glioblastoma.

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“…Monocytes usually originate from myeloid progenitors in the bone marrow. In mice, monocytes are classified into two subsets, the classical Ly-6C high CCR2 high CX3CR1 low and nonclassical Ly-6C low CCR2 low CX3CR1 high subtypes, based on Ly-6C expression levels; the former subtype migrates to the infarcted areas and serves as the main contributor to inflammation, while the latter always persists in the circulation and is responsible for maladaptive remodeling 63 - 65 .…”

Section: Immune Cellsmentioning

confidence: 99%

The Roles of Noncardiomyocytes in Cardiac Remodeling

Yang

Liu

et al. 2020

Int. J. Biol. Sci.

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Cardiac remodeling is a common characteristic of almost all forms of heart disease, including cardiac infarction, valvular diseases, hypertension, arrhythmia, dilated cardiomyopathy and other conditions. It is not merely a simple outcome induced by an increase in the workload of cardiomyocytes (CMs). The remodeling process is accompanied by abnormalities of cardiac structure as well as disturbance of cardiac function, and emerging evidence suggests that a wide range of cells in the heart participate in the initiation and development of cardiac remodeling. Other than CMs, there are numerous noncardiomyocytes (non-CMs) that regulate the process of cardiac remodeling, such as cardiac fibroblasts and immune cells (including macrophages, lymphocytes, neutrophils, and mast cells). In this review, we summarize recent knowledge regarding the definition and significant effects of various non-CMs in the pathogenesis of cardiac remodeling, with a particular emphasis on the involved signaling mechanisms. In addition, we discuss the properties of non-CMs, which serve as targets of many cardiovascular drugs that reduce adverse cardiac remodeling.

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

Cited by 51 publications

References 72 publications

Increased phagocytosis in the presence of enhanced M2-like macrophage responses correlates with increased primary and latent HSV-1 infection

Increased phagocytosis in the presence of enhanced M2-like macrophage responses correlates with increased primary and latent HSV-1 infection

MiR-374b targets GATA3 to promote progression and development of glioblastoma via regulating SEMA3B

The Roles of Noncardiomyocytes in Cardiac Remodeling

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