Effects of benner pury on the function of endothelial progenitor cells in vitro from patients with hypertension in a time-dependent manner

2016 ◽  
Vol 3 (1) ◽  
pp. 5
Author(s):  
Yongdong Li ◽  
Huihua Wen ◽  
Ruizhen Lian ◽  
Gaole Alatan
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Time Dependent ◽  
Dependent Manner ◽  
Endothelial Progenitor

scholarly journals Vitamin D (1,25-(OH)2D3) Improves Endothelial Progenitor Cells Function via Enhanced NO Secretion in Systemic Lupus Erythematosus

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Zhenhua Huang ◽  
Lixiang Liu ◽  
Shufen Huang ◽  
Jianbo Li ◽  
Shaozhen Feng ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Vitamin D ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Lupus Erythematosus ◽  
No Production ◽  
Dependent Manner ◽  
Systemic Lupus ◽  
Endothelial Progenitor

It has been proven that vitamin D was decreased and function of circulating endothelial progenitor cells (EPCs) was injured in systemic lupus erythematosus (SLE) patients. However, the effect of vitamin D on the function of EPCs in vitro and its mechanism need further study. Therefore, we investigated whether vitamin D improved the function of EPCs in vitro. The peripheral blood mononuclear cells of the participants were isolated from SLE patients and control subjects and cultured to EPCs. After the EPCs were treated with vitamin D (1,25-(OH)2D3), we evaluated the number, migratory and proliferative activities, and nitric oxide (NO) production of EPCs in vitro and detected vascular endothelial function by flow-mediated dilatation (FMD). We found that vitamin D in a dose-dependent manner improved number and migratory and proliferative activities of EPCs from SLE patients. Additionally, vitamin D upregulated NO production from EPCs in vitro. A significant correlation between the FMD and plasma NO level was found. There was also a correlation between number, migration, and proliferation of EPCs and NO production. Thus, the present findings indicated that vitamin D improved the function of EPCs from SLE patients via NO secretion.

scholarly journals Aliskiren Improved the Endothelial Repair Capacity of Endothelial Progenitor Cells from Patients with Hypertension via the Tie2/PI3k/Akt/eNOS Signalling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Shun Yao ◽  
Chen Su ◽  
Shao-Hong Wu ◽  
Da-Jun Hu ◽  
Xing Liu
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Signalling Pathway ◽  
Favourable Effect ◽  
Blue Dye ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Repair Capacity

Background. Studies show that aliskiren exerts favourable effects not only on endothelial progenitor cells (EPCs) but also on endothelial function. However, the mechanism of the favourable effect of aliskiren on EPCs from patients with hypertension is unclear and remains to be further studied. Methods. The object of this study was to investigate and assess the in vitro function of EPCs pretreated with aliskiren. After treated with aliskiren, the human EPCs were transplanted into a nude mouse model of carotid artery injury, and the in vivo reendothelialization of injured artery was estimated by staining denuded areas with Evans blue dye via tail vein injection. Results. We found that aliskiren increased the in vitro migration, proliferation, and adhesion of EPCs from patients with hypertension in a dose-dependent manner and improved the reendothelialization capability of these EPCs. Furthermore, aliskiren increased the phosphorylation of Tie2, Akt, and eNOS. After the blockade of the Tie2 signalling pathway, the favourable effects of aliskiren on the in vitro function and in vivo reendothelialization capability of EPCs were suppressed. Conclusions. This study demonstrates that aliskiren can improve the in vitro function and in vivo reendothelialization capability of EPCs from patients with hypertension via the activation of the Tie2/PI3k/Akt/eNOS signalling pathway. These findings further indicate that aliskiren is an effective pharmacological treatment for cell-based repair in hypertension-related vascular injury.

Abstract 332: Cell-Free Conditioned Media From Endothelial Progenitor Cells Enhance Endothelial Angiogenesis, Migration and Survival: Paracrine Implications for Cell Therapy in Pulmonary Arterial Hypertension

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Colin Suen ◽  
Yupu Deng ◽  
Duncan Stewart
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Conditioned Media ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Pulmonary Arterial

Background: Endothelial progenitor cells (EPCs) have been shown to be effective in the prevention of pulmonary arterial hypertension (PAH) in preclinical models. Our group has also demonstrated that xenotransplantation of human early EPCs in the rat monocrotaline (MCT) model prevented pulmonary arterial hypertension, despite the near complete loss of human cells from the lung after even 24 hours. Therefore, we hypothesize that the therapeutic effects of EPCs in PAH are mediated by a paracrine mechanism, which in turn, may enhance endothelial repair and integrity. Methods: EPCs were derived from human peripheral blood mononuclear cells obtained via leukapheresis by adherence to fibronectin and growth in endothelial growth medium (EGM-2MV). 24 hour conditioned medium from Day 6 EPCs (EPC-CM) was collected and concentrated by ultrafiltration prior to in vitro and in vivo studies. PAH was induced by a single intraperitoneal injection of (MCT) in nude athymic rats (150-200 g). EPC (5x106/kg) or EPC-CM from an equivalent number of cells were administered via jugular vein at day 3 after MCT and hemodynamics and echocardiography were assessed at day 24. Results: Incubation of human umbilical vein endothelial cells (ECs) with EPC-CM enhanced Matrigel capillary-like network formation by approximately 2-fold compared with serum-free media (p<0.05). EPC-CM increased migration in the scratch wound-healing assay compared to control media (4-fold, p<0.001). EPC-CM also significantly improved survival of HUVECs after serum deprivation (p<0.05) in a dose-dependent manner. Injection of EPCs resulted in decreased right ventricular systolic pressure (p<0.05) and improvement in pulmonary artery acceleration time (+28%, p<0.05). However, infusion of an equivalent amount of EPC-CM as well as a 10-fold increased dose of EPC-CM failed to prevent PAH. Conclusions: Therefore, EPC-CM enhanced in vitro EC angiogenesis, migration, and survival, consistent with potential of a paracrine mechanism. However, in an in vivo preclinical model, EPC conditioned media did not prevent PAH, suggesting that intact cells act through mechanisms that may involve cell-cell signaling.

Erythropoietin regulates endothelial progenitor cells

Blood ◽  
2004 ◽  
Vol 103 (3) ◽  
pp. 921-926 ◽  
Author(s):  
Ferdinand H. Bahlmann ◽  
Kirsten de Groot ◽  
Jens-Michael Spandau ◽  
Aimee L. Landry ◽  
Barbara Hertel ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Peripheral Blood ◽  
Healthy Subjects ◽  
Tube Formation ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Vitro Assay ◽  
Dose Dependent

AbstractCirculating bone marrow–derived endothelial progenitor cells (EPCs) promote vascular reparative processes and neoangiogenesis, and their number in peripheral blood correlates with endothelial function and cardiovascular risk. We tested the hypothesis that the cytokine erythropoietin (EPO) stimulates EPCs in humans. We studied 11 patients with renal anemia and 4 healthy subjects who received standard doses of recombinant human EPO (rhEPO). Treatment with rhEPO caused a significant mobilization of CD34+/CD45+ circulating progenitor cells in peripheral blood (measured by flow cytometry), and increased the number of functionally active EPCs (measured by in vitro assay) in patients (week 2, 312% ± 31%; week 8, 308% ± 40%; both P &lt; .01 versus baseline) as well as in healthy subjects (week 8, 194% ± 15%; P &lt; .05 versus baseline). The effect on EPCs was already observed with an rhEPO dose of about 30 IU/kg per week. Administration of rhEPO increased the number of functionally active EPCs by differentiation in vitro in a dose-dependent manner, assessed in cell culture and by tube formation assay. Furthermore, rhEPO activates the Akt protein kinase pathway in EPCs. Erythropoietin increases the number of functionally active EPCs in humans. Administration of rhEPO or EPO analogs may open new therapeutic strategies in regenerative cardiovascular medicine.

Gene transfer of endothelial NO-synthase restores migratory capacity of endothelial progenitor cells from patients with coronary artery diseases

2007 ◽  
Vol 30 (4) ◽  
pp. 96
Author(s):  
Michael R. Ward ◽  
Qiuwang Zhang ◽  
Duncan J. Stewart ◽  
Michael J.B. Kutryk
Keyword(s):  
Risk Factors ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Fold Increase ◽  
No Synthase ◽  
Endothelial Progenitor ◽  
Migratory Capacity ◽  
Acute Mi ◽  
Cad Risk

Autologous endothelial progenitor cells (EPCs) have been used extensively in the development of cell-based therapy for acute MI. However, EPCs isolated from patients with CAD and/or CAD risk factors have reduced regenerative activity compared to cells from healthy subjects. As in endothelial cells, endothelial NO synthase (eNOS) expression and subsequent NO production are believed to be critical determinants of EPC function. Recently, the ability of EPCs to migrate in vitro in response to chemotactic stimuli has been shown to predict their regenerative capacity in clinical studies. Therefore, we hypothesized that the regenerative function of EPCs from patients with or at high risk for CAD will be enhanced by overexpression of eNOS, as assessed by migratory capacity. Methods: EPCs were isolated from the blood of human subjects with CAD risk factors (>15% Framingham risk score; FRS) (± CAD) by Ficoll gradient separation and differential culture. Following 3 days in culture, cells were transduced using lentivirus vectors containing either eNOS or GFP (sham) at an MOI of 3. The cells were cultured for an additional 5 days before being used in functional assays. Cell migration and chemotaxis in response to VEGF (50 ng/mL) and SDF-1 (100 ng/mL) were assessed using a modified Boyden Chamber assay. Results: Transduction at an MOI of 3 led to a ~90-100-fold increase in eNOS mRNA expression and a 5-6 fold increase in eNOS protein expression, as assessed by qRT-PCR and Western Blotting. Moreover, there was a significant improvement in the migration of EPCs following eNOS transduction compared to sham-transduced EPCs in response to both VEGF (44.3 ± 8.4 vs. 31.1 ± 4.6 cells/high power field; n=10, p < 0.05) and SDF-1 (51.9 ± 11.1 vs. 34.5 ± 3.3 cells/HPF; n=10, p < 0.05). Conclusions: These data show that the reduced migration capacity of EPCs isolated from patients with CAD and/or CAD risk factors can be significantly improved through eNOS overexpression in these cells. Thus, eNOS transduction of autologous EPCs may enhance their ability to restore myocardial perfusion and function following acute MI. We intend to further explore the regenerative potential of eNOS-transduced EPCs using various in vitro and in vivo models.

scholarly journals Effective Actions of Ion Release from Mesoporous Bioactive Glass and Macrophage Mediators on the Differentiation of Osteoprogenitor and Endothelial Progenitor Cells

Pharmaceutics ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1152
Author(s):  
Alberto Polo-Montalvo ◽  
Laura Casarrubios ◽  
María Concepción Serrano ◽  
Adrián Sanvicente ◽  
María José Feito ◽  
...  
Keyword(s):  
Bone Regeneration ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mesoporous Structure ◽  
Ion Release ◽  
Endothelial Progenitor ◽  
Matrix Mineralization ◽  
Intracellular Content

Due to their specific mesoporous structure and large surface area, mesoporous bioactive glasses (MBGs) possess both drug-delivery ability and effective ionic release to promote bone regeneration by stimulating osteogenesis and angiogenesis. Macrophages secrete mediators that can affect both processes, depending on their phenotype. In this work, the action of ion release from MBG-75S, with a molar composition of 75SiO2-20CaO-5P2O5, on osteogenesis and angiogenesis and the modulatory role of macrophages have been assessed in vitro with MC3T3-E1 pre-osteoblasts and endothelial progenitor cells (EPCs) in monoculture and in coculture with RAW 264.7 macrophages. Ca2+, phosphorous, and silicon ions released from MBG-75S were measured in the culture medium during both differentiation processes. Alkaline phosphatase activity and matrix mineralization were quantified as the key markers of osteogenic differentiation in MC3T3-E1 cells. The expression of CD31, CD34, VEGFR2, eNOS, and vWF was evaluated to characterize the EPC differentiation into mature endothelial cells. Other cellular parameters analyzed included the cell size and complexity, intracellular calcium, and intracellular content of the reactive oxygen species. The results obtained indicate that the ions released by MBG-75S promote osteogenesis and angiogenesis in vitro, evidencing a macrophage inhibitory role in these processes and demonstrating the high potential of MBG-75S for the preparation of implants for bone regeneration.

scholarly journals Interleukin-1β Augments Angiogenic Responses of Murine Endothelial Progenitor Cells in Vitro

2009 ◽  
Vol 29 (5) ◽  
pp. 933-943 ◽  
Author(s):  
Anna Rosell ◽  
Ken Arai ◽  
Josephine Lok ◽  
Tongrong He ◽  
Shuzhen Guo ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Mononuclear Cells ◽  
Therapeutic Angiogenesis ◽  
Interleukin 1Β ◽  
Endothelial Progenitor ◽  
Angiogenic Potential ◽  
Diphenyl Tetrazolium Bromide ◽  
In Vitro Angiogenesis

Endothelial progenitor cells (EPCs) may provide novel opportunities for therapeutic angiogenesis after ischemic diseases. However, it is unclear how the angiogenic potential of EPCs might be affected by an inflammatory environment. We examine how the potent cytokine interleukin-1β (IL-1β) affects angiovasculogenic responses in EPCs in culture. Mononuclear cells isolated from mouse spleen were plated on fibronectin-coated wells and grown in EGM-2 MV media. Endothelial progenitor cells were phenotyped using multiple markers (UEA-Lectin, ac-LDL, CD133, CD34, vWillebrand Factor, Flk-1) and to identify the IL-1 Receptor-I. We quantified cell and colony counts and performed MTT (3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl-tetrazolium bromide) and Matrigel assays, in vitro, under control and IL-1β (10 ng/mL) conditions. Endothelial progenitor cells exposed to IL-1β increased in the number of cells and colonies compared with untreated cells, without any effect on cell metabolic integrity. Furthermore, IL-1β treatment augmented EPC angiogenic function, significantly increasing the number of vessel-like structures in the Matrigel assay. An early phosphorylation of ERK1/2 occurred after IL-1β stimulation, and this pathway was inhibited if IL-1 Receptor-I was blocked. Our results suggest that IL-1β is a potent stimulator of in vitro angiogenesis through ERK signaling in mouse EPCs. Further studies are warranted to assess how interactions between proinflammatory environments and EPC responses may be leveraged to enhance therapeutic angiogenesis.

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