scholarly journals Endothelial progenitor cells in pathogenesis of new coronaviral infection

2021 ◽  
pp. 199-204
Author(s):  
N. A. Kuzubova ◽  
O. N. Titova ◽  
E. S. Lebedeva ◽  
E. V. Volchkova
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Endothelium ◽  
Clinical Manifestations ◽  
Endothelial Progenitor ◽  
Hematopoietic Stem ◽  
Damage Area ◽  
Endothelium Dysfunction ◽  
Pathogenic Factors ◽  
And Migration

Pulmonary vascular endothelium dysfunction is one of the main pathogenic factors responsible for many clinical manifestations of the severe course of COVID-19. Circulating endothelial progenitor cells (EPCs) are the endogenous regenerative reserve that maintains the integrity of the vascular endothelium and its restoration in case of damage by pathogenic factors. A decrease in the circulating EPCs is regarded as a predictor of morbidity and mortality in conditions associated with development of endothelial dysfunction, including COVID-19. The exact phenotype of progenitor cells capable of differentiating into endothelial cells has not been determined. In most laboratories antigens CD133+, CD34+, VEGFR-2+ (CD 309) or combination of these are used to identify EPCs. The process of EPCs mobilization and migration is controlled by molecular signals from immune cells located in the damage area. Stromal cell factor 1 (SDF-1), produced by the bone marrow and many other tissues, is an important chemoattractant for EPCs which express its receptors. The results of studies carried out in 2020 indicate that SARS-Cov-2 infects both hematopoietic stem cells, transforming into EPCs, and directly circulating EPCs, causing inflammatory and procoagulant reactions that complicate the COVID-19 course. There is no consensus on the mechanism of EPCs infection with coronavirus – directly through the expression of angiotensin-converting enzyme (ACE2) receptor or through an ACE2-independent mechanism. Today there is no effective therapy for COVID-19. The use of the EPCs regenerative potential, and the search for ways to enhance the EPCs mobilization from the depot, and increase their functional activity may become a promising approach to the prevention of severe complications and mortality from COVID-19.

scholarly journals Ultrasonic microbubble VEGF gene delivery improves angiogenesis of senescent endothelial progenitor cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi-Nan Lee ◽  
Yih-Jer Wu ◽  
Hsin-I. Lee ◽  
Hsueh-Hsiao Wang ◽  
Chiung-Yin Chang ◽  
...  
Keyword(s):  
Gene Delivery ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Copy Number ◽  
Therapeutic Effects ◽  
Endothelial Progenitor ◽  
Cell Therapies ◽  
Aortic Endothelial Cells ◽  
Angiogenic Effect ◽  
And Migration

AbstractThe therapeutic effects of ultrasonic microbubble transfection (UMT)-based vascular endothelial growth factor 165 (VEGF165) gene delivery on young and senescent endothelial progenitor cells (EPCs) were investigated. By UMT, plasmid DNA (pDNA) can be delivered into both young EPCs and senescent EPCs. In the UMT groups, higher pDNA-derived protein expression was found in senescent EPCs than in young EPCs. Consistent with this finding, a higher intracellular level of pDNA copy number was detected in senescent EPCs, with a peak at the 2-h time point post UMT. Ultrasonic microbubble delivery with or without VEGF improved the angiogenic properties, including the proliferation and/or migration activities, of senescent EPCs. Supernatants from young and senescent EPCs subjected to UMT-mediated VEGF transfection enhanced the proliferation and migration of human aortic endothelial cells (HAECs), and the supernatant of senescent EPCs enhanced proliferation more strongly than the supernatant from young EPCs. In the UMT groups, the stronger enhancing effect of the supernatant from senescent cells on HAEC proliferation was consistent with the higher intracellular VEGF pDNA copy number and level of protein production per cell in the supernatant from senescent cells in comparison to the supernatant from young EPCs. Given that limitations for cell therapies are the inadequate number of transplanted cells and/or insufficient cell angiogenesis, these findings provide a foundation for enhancing the therapeutic angiogenic effect of cell therapy with senescent EPCs in ischaemic cardiovascular diseases.

scholarly journals Very Small Embryonic-Like Stem Cells, Endothelial Progenitor Cells, and Different Monocyte Subsets Are Effectively Mobilized in Acute Lymphoblastic Leukemia Patients after G-CSF Treatment

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Andrzej Eljaszewicz ◽  
Lukasz Bolkun ◽  
Kamil Grubczak ◽  
Malgorzata Rusak ◽  
Tomasz Wasiluk ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Acute Lymphoblastic Leukemia ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Lymphoblastic Leukemia ◽  
Monocyte Subsets ◽  
Endothelial Progenitor ◽  
Hematopoietic Stem ◽  
Cd34 Cells

Background. Acute lymphoblastic leukemia (ALL) is a malignant disease of lymphoid progenitor cells. ALL chemotherapy is associated with numerous side effects including neutropenia that is routinely prevented by the administration of growth factors such as granulocyte colony-stimulating factor (G-CSF). To date, the effects of G-CSF treatment on the level of mobilization of different stem and progenitor cells in ALL patients subjected to clinically effective chemotherapy have not been fully elucidated. Therefore, in this study we aimed to assess the effect of administration of G-CSF to ALL patients on mobilization of other than hematopoietic stem cell (HSCs) subsets, namely, very small embryonic-like stem cells (VSELs), endothelial progenitor cells (EPCs), and different monocyte subsets. Methods. We used multicolor flow cytometry to quantitate numbers of CD34+ cells, hematopoietic stem cells (HSCs), VSELs, EPCs, and different monocyte subsets in the peripheral blood of ALL patients and normal age-matched blood donors. Results. We showed that ALL patients following chemotherapy, when compared to healthy donors, presented with significantly lower numbers of CD34+ cells, HSCs, VSELs, and CD14+ monocytes, but not EPCs. Moreover, we found that G-CSF administration induced effective mobilization of all the abovementioned progenitor and stem cell subsets with high regenerative and proangiogenic potential. Conclusion. These findings contribute to better understanding the beneficial clinical effect of G-CSF administration in ALL patients following successful chemotherapy.

scholarly journals Protective Effect of Silymarin against Rapamycin-induced Apoptosis and Proliferation Inhibition in Endothelial Progenitor Cells

2015 ◽  
Vol 10 (2) ◽  
pp. 1934578X1501000 ◽  
Author(s):  
Peng Zhang ◽  
Guohua Han ◽  
Pei Gao ◽  
Kun Qiao ◽  
Yusheng Ren ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Control Group ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Concentration Dependent Manner ◽  
Inhibition Of Proliferation ◽  
And Migration ◽  
Proliferation And Migration

For this study, peripheral blood samples were collected from human volunteers. Mononuclear cells (MNC) were separated by density centrifugation and were induced to differentiate into endothelial progenitor cells (EPCs) in vitro. Different concentrations of rapamycin and silymarin were introduced to the EPCs over 24 hours and then EPCs were analyzed for proliferation, migration, apoptosis and angiogenesis. Compared with the control group, rapamycin (1, 10, 100 ng/mL) inhibited the proliferation and migration of EPCs in a concentration dependent manner ( P<0.05). Silymarin (50, 100 μg/mL) enhanced the proliferation and migration of EPCs and inhibited apoptosis in a concentration dependent manner ( P<0.05). By adding rapamycin (1 ng/mL) and silymarin (25, 50, 100 μg/mL) over 24 hours, silymarin inhibited the pro-apoptotic effect of rapamycin on EPCs, and reversed the inhibition of proliferation, migration and angiogenesis of EPCs by rapamycin ( P<0.05).

Endothelial Progenitor Cells in Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 2397-2397
Author(s):  
Sophie Gandrille ◽  
Régis Peffault de Latour ◽  
Emeline Levionnois ◽  
Anna D. Petropoulou ◽  
Isabelle Galy-Fauroux ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Gene Mutation ◽  
Paroxysmal Nocturnal Hemoglobinuria ◽  
Cell Activation ◽  
Endothelial Progenitor ◽  
Activation Markers ◽  
Hematopoietic Stem ◽  
Common Precursor

Abstract Abstract 2397 Introduction: Paroxysmal nocturnal hemoglobinuria (PNH), a very rare disease, is characterized by hemolytic anemia, bone marrow failure, and venous thromboembolism. The disease is caused by somatic mutation of the X-linked gene PIG-A encoding a key enzyme responsible for the biosynthesis of the GPI-anchored proteins (GPI-APs), affecting hematopoietic stem cells (HSC). Venous thromboembolisms occur in unusual sites and the mechanism remains to be elucidated. A previous study showed an increase of endothelial cell activation markers in PNH patients (Helley et al., Haematologica 2010;95:574-581), however endothelial cells remain poorly studied in this disease. In polycythemia vera, associating JAK-2 mutation in HSC and thrombosis occurrence, Sozer and coworkers showed that liver endothelial cells bore the same JAK-2 mutation than the HSC (Sozer et al, Blood Cells, Molecules and Diseases, 2009;43:304-312). This suggests the existence of a common precursor between endothelial progenitor cells and HSC, the hemangioblast. In PNH, PIG-A gene mutations might be present in endothelial cells. To test this hypothesis we have used endothelial progenitor cells circulating in blood, also called endothelial-colony forming cells (ECFC), as witnesses of endothelial cells status. Methods: Peripheral blood mononuclear cells (PBMC) and neutrophiles (PMNL), from patients with classical PNH, were fractionated. PMNL were used to isolate DNA, while PBMC were plated on gelatine-coated plates to be cultured until appearance of ECFC colonies (usually 15–20 days), and then cultured to perform: (i) expression of GPI-anchored protein by flow cytometry; (ii) sequencing of the exons and flanking regions of the PIG-A gene from PMNL and ECFC. Results: Twelve PNH patients were enrolled (8 women, 4 men). Among them, 3 have venous thrombotic events (2 Budd-Chiari syndromes and one mesenteric veins thrombosis). ECFC colonies were obtained from 6 out of the 12 patients, a normal output due to the small number of ECFC in whole blood. Mutations identified by sequencing the PIG-A gene of PMNLs from these 6 patients are shown in Table 1, as well as clinical characteristics. In 5 patients only (two with previous Budd-Chiari syndrome), we obtained sufficient amounts of ECFC to isolate DNA. None of the ECFC colonies bore the identified mutations (one exhibited a very faint peak of mutated nucleotide on electrophoregram but mRNA transcripts analysis from this ECFC colony revealed traces amounts of CD45 and CD11b mRNA, suggesting a contamination by leukocytes). Conclusion: This is the first study reporting the absence of PIG-A gene mutation in ECFC from PNH patients, indicating that the mature endothelial cells are not bearing the PIG-A mutation. These cells are thus involved in thrombosis probably by free hemoglobin and thrombin cell activation, rather than by direct damage caused by PIG-A gene mutation. These results also indicate that, in PNH, the PIG-A gene mutation occurs most probably after the common precursor between endothelial progenitor cells and HSC. Disclosures: Peffault de Latour: Alexion: Consultancy, Research Funding. Fischer:Alexion: Consultancy. Helley:Alexion: Consultancy.

Identification of functional endothelial progenitor cells suitable for the treatment of ischemic tissue using human umbilical cord blood

Blood ◽  
2007 ◽  
Vol 110 (1) ◽  
pp. 151-160 ◽  
Author(s):  
Masumi Nagano ◽  
Toshiharu Yamashita ◽  
Hiromi Hamada ◽  
Kinuko Ohneda ◽  
Ken-ichi Kimura ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cord Blood ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Human Umbilical Cord ◽  
Aldh Activity ◽  
Endothelial Progenitor ◽  
Hematopoietic Stem

Umbilical cord blood (UCB) has been used as a potential source of various kinds of stem cells, including hematopoietic stem cells, mesenchymal stem cells, and endothelial progenitor cells (EPCs), for a variety of cell therapies. Recently, EPCs were introduced for restoring vascularization in ischemic tissues. An appropriate procedure for isolating EPCs from UCB is a key issue for improving therapeutic efficacy and eliminating the unexpected expansion of nonessential cells. Here we report a novel method for isolating EPCs from UCB by a combination of negative immunoselection and cell culture techniques. In addition, we divided EPCs into 2 subpopulations according to the aldehyde dehydrogenase (ALDH) activity. We found that EPCs with low ALDH activity (Alde-Low) possess a greater ability to proliferate and migrate compared to those with high ALDH activity (Alde-High). Moreover, hypoxia-inducible factor proteins are up-regulated and VEGF, CXCR4, and GLUT-1 mRNAs are increased in Alde-Low EPCs under hypoxic conditions, while the response was not significant in Alde-High EPCs. In fact, the introduction of Alde-Low EPCs significantly reduced tissue damage in ischemia in a mouse flap model. Thus, the introduction of Alde-Low EPCs may be a potential strategy for inducing rapid neovascularization and subsequent regeneration of ischemic tissues.

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