Endothelial progenitor cells: Origin and role of angiogenesis in cardiovascular diseases

Denisenko, O. A.; Chumakova, S. P.; Уразова, О. И.

doi:10.29001/2073-8552-2021-36-2-23-29

Cited by 6 publications

(3 citation statements)

References 29 publications

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“…SDF-1 accumulation in the plasma stimulates CXCR4 + cell mobilization from the bone marrow, including hematopoietic stem cells and EPCs, which express CXCR4 as a receptor for SDF-1. The SDF-1 and CXCR4 interaction also stimulates the recruitment and retention of stem cells in ischemic areas [13,[17][18][19][20]. Another chemotactic factor, MCP-1, mediates monocytic EPC attachment to the damaged endothelium, which is accompanied by their differentiation into cells expressing endothelial markers (Tie2, CD31 and VE-cadherin) and the inhibition of vascular intimal hyperplasia [21].…”

Section: The Coronary Vessels' Endothelium Desquamation In Icmp Is In...mentioning

confidence: 99%

“…The VEGF-A content in the blood from the coronary sinus exceeded that in the peripheral blood of CHD patients of both groups, likely reflecting the induction of angiogenesis under ischemic conditions (Table 2). VEGF-A binds to VEGFR1 and VEGFR2, stimulating EPC proliferation and differentiation into endothelial cells and the formation of tubular structures and increasing vascular wall permeability, and inhibits cardiomyocyte apoptosis [13,[26][27][28]. Given that hypoxia increases VEGFR1 expression [27], which is a decoy receptor for VEGF-A, may inhibit angiogenesis [28] and activate MMP-9 secretion from vascular myocytes [29], patients with ICMP, due to chronic hypoxia, may present with an attenuation of the interaction between VEGF-A and VEGFR2.…”

Section: The Coronary Vessels' Endothelium Desquamation In Icmp Is In...mentioning

confidence: 99%

“…In this regard, the study of angiogenesis mediators (such as vascular endothelial growth factor (VEGF) −A and −B, platelet-derived growth factor (PDGF), angiopoietin (Ang)-2, macrophage chemotactic factor (MCP)-1 and stromal cell-derived factor (SDF)-1), along with galectin-3 and MMP-9 production in the heart [12,13] can help to establish the mechanisms of angiogenesis and angiopoietic endothelial dysfunction in CHD with and without ICMP. At the same time, the comparison of the monocytic immunophenotype endothelial progenitor cells (EPCs) and endothelial desquamated cells (EDCs) levels in the blood allows the determination of the adequacy of the angiogenesis mechanisms in relation to the severity of endothelial damage within coronary vessels, and the hypoxia-induced factors HIF-1 and HIF-2 balance reveal the features of mediator response of cells to hypoxia in ICMP compared to CHD without cardiomyopathy.…”

Section: Introductionmentioning

confidence: 99%

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Role of Angiopoietic Coronary Endothelial Dysfunction in the Pathogenesis of Ischemic Cardiomyopathy

et al. 2023

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Background: The angiopoietic endothelial dysfunction in ischemic cardiomyopathy (ICMP) remains unexplored. Aim: The identification of the imbalance of endothelial dysfunction mediators and the number of endothelial progenitor (EPC) and desquamated (EDC) cells in patients with coronary heart disease (CHD) with and without ICMP. Methods: A total of 87 patients (47 with ICMP and 40 without ICMP) were observed. The content of EPCs (CD14+CD34+VEGFR2+) in vein blood and EDCs (CD45−CD146+) in the blood from the coronary sinus and cubital vein was determined by flow cytometry. The contents of HIF-1α and HIF-2α in vein blood as well as that of ADMA and endothelin-1 in sinus plasma and angiopoietin-2, MMP-9 and galectin-3 in both samples were assessed using ELISA, and VEGF, PDGF, SDF-1 and MCP-1 contents using immunofluorescence. Results: ADMA and endothelin-1 levels in the sinus blood were comparable between the patient groups; a deficiency of HIF-1α and excess of HIF-2α were detected in the vein blood of ICMP patients. The EDC content in the vein blood increased in CHD patients regardless of ICMP, and the concentrations of VEGF-A, VEGF-B, PDGF, MCP-1, angiopoietin-2, and MMP-9 were normal. In ICMP patients, vein blood was characterized by an excess of galectin-3 and sinus blood by an excess of EDCs, angiopoietin-2, MMP-9 and galectin-3. Conclusion: ICMP is accompanied by angiopoietic endothelial dysfunction.

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Section: The Coronary Vessels' Endothelium Desquamation In Icmp Is In...mentioning

confidence: 99%

Section: The Coronary Vessels' Endothelium Desquamation In Icmp Is In...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of Angiopoietic Coronary Endothelial Dysfunction in the Pathogenesis of Ischemic Cardiomyopathy

et al. 2023

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The Role of Angiogenesis Mediators in the Mobilization of Early and Late Endothelial Progenitor Cells from the Bone Marrow in Coronary Heart Disease

Chumakova,

Urazova,

Shipulin

et al. 2024

Annals RAMS

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Background. A severe form of coronary heart disease (CHD) is ischemic cardiomyopathy (ICMP), the pathogenesis of which has not been fully studied. Disturbances in the mobilization of endothelial progenitor cells (EPC) due to an imbalance of angiogenesis mediators may exacerbate ischemia in ICMP. The aim — to establish the peculiarities of changes in the balance of early and late EPС and subpopulations of VEGFR2+ cells in the blood and bone marrow in relation to the content of angiogenesis mediators and the number of desquamated endothelial cells (DEK) in the blood of patients with CHD, suffering and not suffering from ICMP. Methods. A single-stage, clinical, controlled (case-control) study was conducted from March 2019 to June 2022. 52 patients with CHD who had a history of myocardial infarction were examined: 30 people suffering from ICMP and 22 people not suffering from ICMP, as well as 15 healthy donors. The content of VEGFR2+, VEGFR2+CD34+CD14+ (early EPC), VEGFR2+CD34+CD14– (late EPC), VEGFR2+CD34–CD14+, VEGFR2+CD34–CD14– cells in patients with CHD in the blood (before surgery) and bone marrow (sampling was performed at the beginning of coronary bypass) and in healthy individuals in the blood, as well as (in both groups) the content of CD45–CD146+ DEC in the blood was determined by flow cytometry. The concentration of SDF-1, VEGF-A, MCP-1, GM-CSF, G-CSF in blood plasma was measured by multiplex immunofluorescence analysis. Results. The development of CHD without cardiomyopathy was accompanied by an increase in the content of VEGFR2+CD34+CD14+ and VEGFR2+ cells (0.74 [0.46; 1.23]% and 10.00 [8.20; 11.60]%, respectively, versus 0.19 [0.13; 0.32]%, p 0.001 and 5.40 [4.30; 6.50]%, p = 0.005) and concentrations of SDF-1, MCP-1, GM-CSF (respectively 60.00 [50.00; 81.00] pg/ml; 223.0 [180.0; 297.0] pg/ml; 2.10 [1.45; 3.40] pg/ml versus 30.00 [5.00; 45.00] pg/ml, p = 0.041; 175.1 [140.0; 204.0] pg/ml, p = 0.046; 0.96 [0.46; 1.41] pg/ml, p = 0.038) in the blood relative to the norm. No such changes were observed in patients with ICMP. Regardless of the presence of ICMP, the content of VEGFR2+CD34+CD14–, VEGFR2+CD34–CD14+, VEGFR2+CD34–CD14– cells, VEGF-A, G-CSF in the blood of patients with CHD varied within physiological values, and the number of DEC exceeded the norm (7.26 [5.43; 17.94]×105/l, p = 0.039). The number of VEGFR2+ cells and their immunophenotypes in the bone marrow of patients with ICMP did not differ from the parameters in patients with CHD without cardiomyopathy. Prolonged bleeding from the venopuncture area was registered in one CHD patient without cardiomyopathy. Conclusion. The development of ICMP is associated with the absence of a compensatory response to atherogenesis in the form of increased mobilization of early EPC from the bone marrow due to the absence of a reaction associated with hyperproduction of SDF-1, MCP-1, GM-CSF, which is characteristic of CHD without cardiomyopathy. The content of EPС, VEGFR2+CD34–CD14+ and VEGFR2+CD34–CD14– cells, VEGF-A and G-CSF in the blood in СHD corresponds to physiological values, regardless of the presence of ICMP. The generation of EPC in the bone marrow in ICMP is not impaired.

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Blood monocytes in maintaining the balance of vascular endothelial injury and repair process in ischemic cardiomyopathy

Chumakova

Уразова

Denisenko³

et al. 2022

Kompleks. probl. serdečno-sosud. zabol.

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Highlights. The features of subsets of monocytes in combination with the levels of desquamated endotheliocytes, endothelial damage and regeneration mediators and progenitor cell migration-enhancing factors in patients with coronary heart disease and with/without ischemic cardiomyopathy were analyzed. For the first time it was shown that in patients with ischemic cardiomyopathy, compared with CHD patients without cardiomyopathy, higher desquamation of the endothelium is associated with a deficiency of non-classical monocytes and reduced migration of progenitor endothelial cells (VEGFR2+-monocytes) with regenerative potential across the bone marrow due to a deficiency of the HIF-1α mediator in the blood.Background. The development of ischemic cardiomyopathy (ICM) is an understudied process, and one of its elements may be insufficient regeneration of blood vessels due to an imbalance of subsets of monocytes in the blood.Aim. To assess subsets of monocytes and desquamated endothelial cells in combination with endothelial damage and regeneration mediators in the blood of patients with coronary heart disease (CHD) and with/without ICM.Methods. The study included 30 patients with ICM, 22 patients with coronary heart disease without cardiomyopathy aged 55–69 years, and 18 healthy donors. In whole blood, the populations of CD45–CD146+ desquamated endothelial cells and progenitor endothelial cells related to CD14+VEGFR2+ monocytes, intermediate CD14++CD16+ and non-classical CD14+CD16++ monocytes were assessed by flow cytometry using the appropriate monoclonal antibodies (BD Biosciens, USA). In blood plasma, the levels of hypoxia-inducible factor HIF-1α, monocyte chemoattractant protein MCP-1 and matrix metalloproteinase MMP-9 were assessed by enzyme immunoassay. The results of the analysis were considered significant at p<0.05.Results. The number of progenitor and desquamated endothelial cells was increased in both groups of patients with coronary artery disease. At the same time, in patients with ICM, the number of progenitor endothelial cells did not reach the number noted in patients with CHD without cardiomyopathy, while the number of desquamated endothelial cells reached the number noted in CHD patients without cardiomyopathy. There was a deficiency of non-classical monocytes and HIF-1α in the blood of patients with ICM, and an excess of intermediate monocytes and MCP-1 was observed in CHD patients without cardiomyopathy. The concentration of MMP-9 in patients with CHD corresponded to the norm, regardless of the presence of ICM.Conclusion. In ICM, in contrast to CHD without cardiomyopathy, vascular damage is associated with a deficiency of nonclassical monocytes and reduced endothelial repair due to insufficient migration of progenitor endothelial cells across the bone marrow due to HIF-1α deficiency in the blood.

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Endothelial progenitor cells: Origin and role of angiogenesis in cardiovascular diseases

Cited by 6 publications

References 29 publications

Role of Angiopoietic Coronary Endothelial Dysfunction in the Pathogenesis of Ischemic Cardiomyopathy

Role of Angiopoietic Coronary Endothelial Dysfunction in the Pathogenesis of Ischemic Cardiomyopathy

The Role of Angiogenesis Mediators in the Mobilization of Early and Late Endothelial Progenitor Cells from the Bone Marrow in Coronary Heart Disease

Blood monocytes in maintaining the balance of vascular endothelial injury and repair process in ischemic cardiomyopathy

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