Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Kim, Yevgeniy; Nurakhayev, Sanzhar; Nurkesh, Ayan; Zharkinbekov, Zharylkasyn; Saparov, Arman

doi:10.3390/ijms22052715

Cited by 86 publications

(104 citation statements)

References 111 publications

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“…PTPRE-AS1 deficiency enhanced PTPRE expression by regulating WDR5-dependent H3K4me3 and, hence, promoted IL-4-stimulated M2 macrophage polarization [ 25 ]. Reparative M2 macrophages have been found to be involved in tumor proliferation and fibrosis [ 26 ]. We found that the expression of PTPRE-AS1 significantly decreased in Hdc −/− mice post MI and increased in RAW264.7 with histamine treatment, which implied that PTPRE-AS1 may play a role in monocyte/macrophage-dependent susceptibility to carcinogenesis [ 6 ] and heart fibrosis [ 10 ] in Hdc −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Immune Associated Co-Expression Networks Reveals Immune-Related Long Non-Coding RNAs during MI in the Presence and Absence of HDC

Zhang

Ding

Yang

et al. 2021

IJMS

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Myocardial infarction (MI) is one of the most common cardiovascular diseases. Although previous studies have shown that histidine decarboxylase (HDC), a histamine-synthesizing enzyme, is involved in the stress response and heart remodeling after MI, the mechanism underlying it remains unclear. In this study, using Hdc-deficient mice (Hdc−/− mice), we established an acute myocardial infarction mouse model to explore the potential roles of Hdc/histamine in cardiac immune responses. Comprehensive analysis was performed on the transcriptomes of infarcted hearts. Differentially expressed gene (DEG) analysis identified 2126 DEGs in Hdc-deficient groups and 1013 in histamine-treated groups. Immune related pathways were enriched in Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Then we used the ssGSEA algorithm to evaluate 22 kinds of infiltrated immunocytes, which indicated that myeloid cells and T memory/follicular helper cells were tightly regulated by Hdc/histamine post MI. The relationships of lncRNAs and the Gene Ontology (GO) functions of protein-coding RNAs and immunocytes were dissected in networks to unveil immune-associated lncRNAs and their roles in immune modulation after MI. Finally, we screened out and verified four lncRNAs, which were closely implicated in tuning the immune responses after MI, including ENSMUST00000191157, ENSMUST00000180693 (PTPRE-AS1), and ENSMUST-00000182785. Our study highlighted the HDC-regulated myeloid cells as a driving force contributing to the government of transmission from innate immunocytes to adaptive immunocytes in the progression of the injury response after MI. We identified the potential role of the Hdc/histamine-lncRNAs network in regulating cardiac immune responses, which may provide novel promising therapeutic targets for further promoting the treatment of ischemic heart disease.

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Section: Discussionmentioning

confidence: 99%

Analysis of Immune Associated Co-Expression Networks Reveals Immune-Related Long Non-Coding RNAs during MI in the Presence and Absence of HDC

Zhang

Ding

Yang

et al. 2021

IJMS

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“…The former type is more capable of differentiating into M1 macrophages, which propagate inflammation, while the latter subset of monocytes gives rise mostly to reparative M2 macrophages ( Figure 1 ). Nevertheless, as with other tissues, an attempt to describe skin macrophages as M1 and M2 phenotypes is probably an oversimplification since a wider range of phenotypes exist [ 67 , 68 ].…”

Section: Acute Wound Healingmentioning

confidence: 99%

Immunology of Acute and Chronic Wound Healing

et al. 2021

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Skin wounds greatly affect the global healthcare system, creating a substantial burden on the economy and society. Moreover, the situation is exacerbated by low healing rates, which in fact are overestimated in reports. Cutaneous wounds are generally classified into acute and chronic. The immune response plays an important role during acute wound healing. The activation of immune cells and factors initiate the inflammatory process, facilitate wound cleansing and promote subsequent tissue healing. However, dysregulation of the immune system during the wound healing process leads to persistent inflammation and delayed healing, which ultimately result in chronic wounds. The microenvironment of a chronic wound is characterized by high quantities of pro-inflammatory macrophages, overexpression of inflammatory mediators such as TNF-α and IL-1β, increased activity of matrix metalloproteinases and abundance of reactive oxygen species. Moreover, chronic wounds are frequently complicated by bacterial biofilms, which perpetuate the inflammatory phase. Continuous inflammation and microbial biofilms make it very difficult for the chronic wounds to heal. In this review, we discuss the role of innate and adaptive immunity in the pathogenesis of acute and chronic wounds. Furthermore, we review the latest immunomodulatory therapeutic strategies, including modifying macrophage phenotype, regulating miRNA expression and targeting pro- and anti-inflammatory factors to improve wound healing.

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“…This presented as reinforced connective tissue structure formation, enhanced microvascular growth, and impaired cardiomyocyte hypertrophy [53]. Many other approaches, including transplantation with human umbilical cord blood mesenchymal stem cells [54] or injection of exosomes from adipose-derived mesenchymal stem cells [55], have been used to promote M2 macrophage polarisation post-MI and resulted in improved cardiac tissue repair in MI models (see review [56]).…”

Section: Monocyte/macrophages: Cells Involved In Both Inflammation and Its Resolutionmentioning

confidence: 99%

Lymphatic Clearance of Immune Cells in Cardiovascular Disease

Ravaud

Ved

Jackson

et al. 2021

Cells

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Recent advances in our understanding of the lymphatic system, its function, development, and role in pathophysiology have changed our views on its importance. Historically thought to be solely involved in the transport of tissue fluid, lipids, and immune cells, the lymphatic system displays great heterogeneity and plasticity and is actively involved in immune cell regulation. Interference in any of these processes can be deleterious, both at the developmental and adult level. Preclinical studies into the cardiac lymphatic system have shown that invoking lymphangiogenesis and enhancing immune cell trafficking in ischaemic hearts can reduce myocardial oedema, reduce inflammation, and improve cardiac outcome. Understanding how immune cells and the lymphatic endothelium interact is also vital to understanding how the lymphatic vascular network can be manipulated to improve immune cell clearance. In this Review, we examine the different types of immune cells involved in fibrotic repair following myocardial infarction. We also discuss the development and function of the cardiac lymphatic vasculature and how some immune cells interact with the lymphatic endothelium in the heart. Finally, we establish how promoting lymphangiogenesis is now a prime therapeutic target for reducing immune cell persistence, inflammation, and oedema to restore heart function in ischaemic heart disease.

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Macrophage Polarization in Cardiac Tissue Repair Following Myocardial Infarction

Cited by 86 publications

References 111 publications

Analysis of Immune Associated Co-Expression Networks Reveals Immune-Related Long Non-Coding RNAs during MI in the Presence and Absence of HDC

Analysis of Immune Associated Co-Expression Networks Reveals Immune-Related Long Non-Coding RNAs during MI in the Presence and Absence of HDC

Immunology of Acute and Chronic Wound Healing

Lymphatic Clearance of Immune Cells in Cardiovascular Disease

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