Trained Circulating Monocytes in Atherosclerosis: Ex Vivo Model Approach

Nikiforov, Nikita G.; Wetzker, Reinhard; Kubekina, M.; Петухова, А. В.; Kirichenko, Tatiana V.; Orekhov, Alexander N.

doi:10.3389/fphar.2019.00725

Cited by 9 publications

(6 citation statements)

References 46 publications

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“…In addition, changes in monocyte inflammatory activation may hinder the resolution of inflammation in atherosclerotic lesions and contribute to disease progression. [ 17 ] Canpolat et al showed that the monocyte count was significantly higher in the CSFP group than in the normal control group. [ 4 ] Our findings are consistent with those of earlier studies.…”

Section: Discussionmentioning

confidence: 99%

Clinical characteristics in patients with coronary slow flow phenomenon

et al. 2021

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Coronary slow flow phenomenon (CSFP) is a coronary artery disease in which coronary angiography shows no obvious stenosis, but there is a delay in blood flow perfusion. The etiopathogenic mechanisms of CSFP are still unclear. The aim of the present study was to investigate the role of clinical characteristics in patients with CSFP, and to provide a reference for exploring the potential mechanisms of CSFP. Patients with angiographically normal epicardial arteries were enrolled (145 patients with CSFP and 145 normal controls). Collected clinical information and laboratory indexes, which measured by peripheral venous blood samples before coronary angiography. Logistic regression analysis was performed for statistical analysis. The present study found 19 clinical and laboratory indexes with statistical differences between the two groups in univariate analysis. Multivariate analysis showed that monocyte count, haemoglobin, serum creatinine and globulin were independent predictors of CSFP. Moreover, the monocyte count, haemoglobin, creatinine and globulin levels were significantly higher in the CSFP patients than the controls, with positive associations between these parameters and the extent of CSFP. In addition, ROC analysis showed the diagnostic value of the above indexes for CSFP.

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Section: Discussionmentioning

confidence: 99%

Clinical characteristics in patients with coronary slow flow phenomenon

et al. 2021

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“…Monocyte polarization plays a key role in the progression of various inflammatory diseases such as atherosclerosis, myocardial infarction, and diabetic cardiomyopathy [236][237][238]. Infiltrated monocyte differentiation depends on the tissue microenvironment they reside in and the external stimuli they receive [239].…”

Section: Bmp-7 Differentiates Monocytes Into M2 Macrophages In Heart mentioning

confidence: 99%

The Role of Bone Morphogenetic Protein 7 (BMP-7) in Inflammation in Heart Diseases

Narasimhulu

Singla

2020

Cells

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Bone morphogenetic protein-7 is (BMP-7) is a potent anti-inflammatory growth factor belonging to the Transforming Growth Factor Beta (TGF-β) superfamily. It plays an important role in various biological processes, including embryogenesis, hematopoiesis, neurogenesis and skeletal morphogenesis. BMP-7 stimulates the target cells by binding to specific membrane-bound receptor BMPR 2 and transduces signals through mothers against decapentaplegic (Smads) and mitogen activated protein kinase (MAPK) pathways. To date, rhBMP-7 has been used clinically to induce the differentiation of mesenchymal stem cells bordering the bone fracture site into chondrocytes, osteoclasts, the formation of new bone via calcium deposition and to stimulate the repair of bone fracture. However, its use in cardiovascular diseases, such as atherosclerosis, myocardial infarction, and diabetic cardiomyopathy is currently being explored. More importantly, these cardiovascular diseases are associated with inflammation and infiltrated monocytes where BMP-7 has been demonstrated to be a key player in the differentiation of pro-inflammatory monocytes, or M1 macrophages, into anti-inflammatory M2 macrophages, which reduces developed cardiac dysfunction. Therefore, this review focuses on the molecular mechanisms of BMP-7 treatment in cardiovascular disease and its role as an anti-fibrotic, anti-apoptotic and anti-inflammatory growth factor, which emphasizes its potential therapeutic significance in heart diseases.

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“…Using RNA-seq data (GSE41690), transcriptomic alterations in PBMs from periodontitis patients were compared with PBMs of periodontal healthy subjects [9]. In case of atherosclerosis, PBMs are reported to be in an activated state and respond more strongly against lipopolysaccharide (LPS) stimulation, showing the increased expression of inflammatory mediators [10]. A publicly available microarray dataset (GSE23746) pertains to transcriptomic aberrations occurring in the PBMs of atherosclerosis patients versus the systemically healthy subjects.…”

Section: Introductionmentioning

confidence: 99%

Shared Molecular Mechanisms between Atherosclerosis and Periodontitis by Analyzing the Transcriptomic Alterations of Peripheral Blood Monocytes

Ning

et al. 2021

Computational and Mathematical Methods in Medicine

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Objective. This study investigated the nature of shared transcriptomic alterations in PBMs from periodontitis and atherosclerosis to unravel molecular mechanisms underpinning their association. Methods. Gene expression data from PBMs from patients with periodontitis and those with atherosclerosis were each downloaded from the GEO database. Differentially expressed genes (DEGs) in periodontitis and atherosclerosis were identified through differential gene expression analysis. The disease-related known genes related to periodontitis and atherosclerosis each were downloaded from the DisGeNET database. A Venn diagram was constructed to identify crosstalk genes from four categories: DEGs expressed in periodontitis, periodontitis-related known genes, DEGs expressed in atherosclerosis, and atherosclerosis-related known genes. A weighted gene coexpression network analysis (WGCNA) was performed to identify significant coexpression modules, and then, coexpressed gene interaction networks belonging to each significant module were constructed to identify the core crosstalk genes. Results. Functional enrichment analysis of significant modules obtained by WGCNA analysis showed that several pathways might play the critical crosstalk role in linking both diseases, including bacterial invasion of epithelial cells, platelet activation, and Mitogen-Activated Protein Kinases (MAPK) signaling. By constructing the gene interaction network of significant modules, the core crosstalk genes in each module were identified and included: for GSE23746 dataset, RASGRP2 in the blue module and VAMP7 and SNX3 in the green module, as well as HMGB1 and SUMO1 in the turquoise module were identified; for GSE61490 dataset, SEC61G, PSMB2, SELPLG, and FIBP in the turquoise module were identified. Conclusion. Exploration of available transcriptomic datasets revealed core crosstalk genes (RASGRP2, VAMP7, SNX3, HMGB1, SUMO1, SEC61G, PSMB2, SELPLG, and FIBP) and significant pathways (bacterial invasion of epithelial cells, platelet activation, and MAPK signaling) as top candidate molecular linkage mechanisms between atherosclerosis and periodontitis.

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Trained Circulating Monocytes in Atherosclerosis: Ex Vivo Model Approach

Cited by 9 publications

References 46 publications

Clinical characteristics in patients with coronary slow flow phenomenon

Clinical characteristics in patients with coronary slow flow phenomenon

The Role of Bone Morphogenetic Protein 7 (BMP-7) in Inflammation in Heart Diseases

Shared Molecular Mechanisms between Atherosclerosis and Periodontitis by Analyzing the Transcriptomic Alterations of Peripheral Blood Monocytes

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