scholarly journals Experimental Study on the Effect of Allogeneic Endothelial Progenitor Cells on Wound Healing in Diabetic Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Min Leng ◽  
Ying Peng ◽  
Manchang Pan ◽  
Hong Wang
Keyword(s):  
Bone Marrow ◽  
Wound Healing ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Healing Process ◽  
Control Group ◽  
Molecular Characteristics ◽  
Diabetic Mice ◽  
Endothelial Progenitor ◽  
Significant Difference

Endothelial progenitor cells (EPCs) are involved in the neovascularization in traumatic and ischemic sites, but EPCs are “detained” in bone marrow under diabetic conditions, which results in reduction of the number of EPCs and their biological activity in peripheral blood. Based on our previous study to mobilize autologous bone marrow EPCs by administering AMD3100+G-CSF to realize the optimal effect, our present study is aimed at exploring the effects of transplanting EPCs locally in a wound model of diabetic mice. First, we prepared and identified EPCs, and the biological functions and molecular characteristics were compared between EPCs from DB/+ and DB/DB mice. Then, we performed full-thickness skin resection in DB/DB mice and tested the effect of local transplantation of EPCs on skin wound healing. The wound healing process was recorded using digital photographs. The animals were sacrificed on postoperative days 7, 14, and 17 for histological and molecular analysis. Our results showed that DB/+ EPCs were biologically more active than those of DB/DB EPCs. When compared with the control group, local transplantation of EPCs accelerated wound healing in DB/DB mice by promoting wound granulation tissue formation, angiogenesis, and collagen fiber deposition, but there was no significant difference in wound healing between DB/+ EPCs and DB/DB EPCs transplanted into the wound. Furthermore, local transplantation of EPCs promoted the expression of SDF-1, CXCR4, and VEGF. We speculated that EPC transplantation may promote wound healing through the SDF-1/CXCR4 axis. This point is worth exploring further. Present data are of considerable significance because they raise the possibility of promoting wound healing by isolating autologous EPCs from the patient, which provides a new approach for the clinical treatment of diabetic wounds in the future.

scholarly journals Vasculoprotective Effects of Combined Endothelial Progenitor Cells and Mesenchymal Stem Cells in Diabetic Wound Care: Their Potential Role in Decreasing Wound-Oxidative Stress

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Supakanda Sukpat ◽  
Nipan Isarasena ◽  
Jutamas Wongphoom ◽  
Suthiluk Patumraj
Keyword(s):  
Stem Cells ◽  
Wound Healing ◽  
Mesenchymal Stem Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Wound Care ◽  
Control Group ◽  
Diabetic Mice ◽  
Mice Model ◽  
Endothelial Progenitor

To investigate whether the combined endothelial progenitor cells (EPCs) and mesenchymal stem cells (MSCs) could enhance angiogenesis and wound healing in diabetic mice. Balb/c nude mice were divided into five groups, including a control group, diabetic group (DM), DM injected with 1 × 106  cells MSCs, DM injected with 1 × 106  cells EPCs, and DM injected with combined 0.5 × 106  cells MSCs and 0.5 × 106  cells EPCs. After seven weeks, the mice were anesthetized, and bilateral full-thickness excision skin wounds were made on the dorsorostral back. The percentage of wound closure in DM group decreased significantly than in control and all other treated groups on day 7 and day 14 (P<0.005). On day 14, the percentage of capillary vascularity in combine-treated group was significantly higher than in DM (P<0.005). In the present study, we have demonstrated that the combined EPCs and MSCs can increase vascular endothelial growth factor (VEGF) level and angiogenesis which resulted in reduced neutrophil infiltration, decreased malondialdehyde (MDA) levels, and enhanced wound healing in diabetic mice model.

Circulating Endothelial Progenitor Cells and Their Relation to Thrombosis in Paroxysmal Nocturnal Hemoglobinuria

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 4535-4535
Author(s):  
Esra Turan Erkek ◽  
Esra Nazligul ◽  
Meliha Nalcaci ◽  
Melih Aktan ◽  
Mustafa Nuri Yenerel
Keyword(s):  
Aplastic Anemia ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Control Group ◽  
Endothelial Progenitor ◽  
Chi Square ◽  
Hematopoietic Stem ◽  
Significant Difference ◽  
Chi Square Test ◽  
History Of

Abstract Introduction: Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired clonal hematopoietic stem cell disorder. Chronic intravascular hemolytic anemia, bone marrow failure and thrombophilia are the main clinical findings. Thrombosis is one of the most important cause of morbidity and mortality of this disease. Multiple factors are held responsible for thrombotic tendency in these patients. Endothelial progenitor cells (EPCs) originate from primitive hematopoietic stem cells and are able to turn into endothelial cells. There are extremely small numbers of EPCs in the circulation under normal conditions. The level of EPCs is considered to be indicative of restoration capacity in case of vascular disease and potential damage. Lower EPC levels are also considered as a risk factor in cardiovascular diseases. In this study, our aim was to investigate circulating EPCs in PNH and their relationship with thrombosis. Seventeen patients with PNH, 18 patients with aplastic anemia and 10 healthy volunteers were included in the study. CD309, CD133 and CD34 antibodies were used in order to determine circulating EPCs by flow cytometry and cells which expressed all three antibodies were analyzed as EPC. Prepared samples were read using a prepared list mode software for endothelial progenitor cells on FACS Diva software in BD FACS Canto II device with 6 color lasers and a total of 1,000,000 cells per analysis were evaluated. EPC levels were compared between untreated PNH patients and who were on eculizumab therapy. Statistical analysis was performed using SPSS 22.0 software. The distribution of variables was evaluated by Kolmogorov-Smirnov test, the analysis of quantitative data was evaluated by ANOVA, Kruskal-Wallis, Mann-Whitney U tests and the analysis of the qualitative data was evaluated by chi-square test. Findings and Discussion: The thrombotic complications were observed in five PNH patients. All of these patients had a history of portal vein thrombosis. One of them also had a history of peripheral arterial disease and amputation related to this. There was not a significant difference in EPC levels between patients with and without a history of thrombosis (p>0,05). We also did not find any significant difference between levels of EPC's in PNH groups with or without eculizumab therapy (p˃0,05). There was no significant difference in levels of EPC between aplastic anemia and PNH groups (p ˃ 0,05). However, we found a significant positive correlation between the levels of EPC and LDH in multivariate analysis (p < 0,05). This finding suggests that hemolysis causes vascular endothelium and promotes new blood vessel formations. Increased EPCs in PNH might be an indirect indicator for vascular endothelium damage in PNH. Table. General Features and Rates of EPC of PNH, AA, Healthy Volunteers Groups Aplastic Anemia group PNH group Control group p Age mean±s.smedian (min-max) 40.0±14.7 37.5 (20.0-67.0) 41.9±13.9 43.0 (19.0-78.0) 29.3±3.5 29.5(24.0-34.0) 0.047 Sex Female n-% Male n-% 7 38,9% 11 61.1% 9 52.9% 8 47.1% 5 50% 5 50% 0.687 EPC(%) mean±s.s median (min-max) 0.2% 0.2% 0.1% (0.0-0.6%) 0.3%±0.3% 0.1% (0.0-0.9%) 0.1%±0.0% %0,0(%0,0-0,2) 0.393 All Events (x1000) mean±s.s median (min-max) 617±172* 565 (360-914) 588±255* 471 (250-1000) 878±143 950(655-1000) 0.003 CD309 and CD34 mean±s.s median (min-max) 0.003±0.002 0.002 (0.001-0.007) 0.005±0.004 0.000-0.011) 0.001±0.001 0.001 (0.000-0.002) 0.009 CD133 mean±s.s median (min-max) 45.8±36.3 58.3 (0.0-88.2) 45.8±39.6 60 (0.0-94.7) 42.0±19.4 46.4 (11.1-81.3) 0.867 ANOVA / Kruskal-Wallis / Mann-Whitney U test / Chi-square test *The difference with the control group, p <0.05 EPCs: Endothelial progenitor cells Disclosures Yenerel: Alexion: Membership on an entity's Board of Directors or advisory committees, Speakers Bureau.

scholarly journals Bone Marrow-Derived Endothelial Progenitor Cells Contribute to Monocrotaline-Induced Pulmonary Arterial Hypertension in Rats via Inhibition of Store-Operated Ca2+ Channels

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ran Miao ◽  
Jun Wan ◽  
Jie Liu ◽  
Jason X.-J. Yuan ◽  
Jing Wang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Right Ventricular ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Control Group ◽  
Trpc Channels ◽  
Endothelial Progenitor ◽  
Pulmonary Arterial

Purpose. This study aimed to explore whether bone marrow- (BM-) derived endothelial progenitor cells (EPCs) contributing to monocrotaline- (MCT-) induced pulmonary arterial hypertension (PAH) in rats via modulating store-operated Ca2+ channels (SOC). Methods. Sprague Dawley (SD) rats were assigned into MCT group (n = 30) and control group (n = 20). Rats in MCT group were subcutaneously administered with 60 mg/kg MCT solution, and rats in control group were injected with equal amount of vehicle. After 3 weeks of treatment, right ventricular systolic pressure (RVSP) and right ventricular hypertrophy index (RVHI) of two groups were measured, and BM-derived EPCs were isolated. Immunochemistry identification and vasculogenesis detection of EPCs were then performed. Ca2+cyt measurement was performed to detect store-operated calcium entry (SOCE) in two groups, followed by determination of Orai and canonical transient receptor potential (TRPC) channels expression. Results. After 3 weeks of treatment, there were significant increases in RVSP and RVHI in MCT group compared with control group, indicating that MCT successfully induced PAH in rats. Moreover, the SOCE (Ca2+cyt rise) in BM-derived EPCs of MCT group was lower than that of control group. Furthermore, the expression levels of Orai3, TRPC1, TRPC3, and TRPC6 in BM-derived EPCs were decreased in MCT group in comparison with control group. Conclusions. The SOC activities were inhibited in BM-derived EPCs of MCT-treated rats. These results may be associated with the depressed expression of Orai3, TRPC1, TRPC3, and TRPC6, which are major mediators of SOC.

Comparative Analysis of the Rabbit Endothelial Progenitor Cells from Bone Marrow and Peripheral Blood Treated with Selenium Nanoparticles

2020 ◽  
Vol 20 ◽  
Author(s):  
Sara Shoeibi
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Real Time ◽  
Endothelial Progenitor Cells ◽  
Selenium Nanoparticles ◽  
Control Group ◽  
Endothelial Progenitor ◽  
Expression Levels ◽  
Anti Inflammatory

Background: Selenium nanoparticles (Se-NPs) are known for their antioxidant and anti-inflammatory activities, which are effective in preventing oxidative damage and improving physiological processes. Objectives: This study aimed at investigating the effects of biosynthesized Se-NPs on bone marrow-derived endothelial progenitor cells (bone marrow-derived EPCs) and blood-derived endothelial progenitor cells (blood-derived EPCs) isolated from rabbits in vitro. Methods: The cultured EPCs incubated with biosynthesized Se-NPs at the concentrations of 0.19, 0.38, 0.76, 1.71, 3.42, 7.03, 14.25, 28.50, 57, 114, and 228 μg/ml for 48 h. After screening of the proliferative potential of the Se-NPs by the MTT assay, the best concentrations were selected for real-time quantitative polymerase chain reaction (RT-qPCR). Real-time quantification of vascular cell adhesion molecule 1 (VCAM-1), lectin-like oxidized low-density lipoprotein (LDL) receptor-1 (LOX-1), endothelial nitric oxide synthase (eNOS), and monocyte chemoattractant protein-1 (MCP-1) gene expressions were analyzed by normalizing with glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as an endogenous reference gene. Results: Blood-derived EPCs and bone marrow-derived EPCs showed morphological differences before treatment in vitro. Se-NPs treated EPCs indicated a significant dose-dependent proliferative activity (P<0.01). In general, the expression levels of VCAM-1, LOX1, and MCP-1 mRNA were significantly decreased (p<0.01), whereas that of the eNOS expression was significantly increased at the concentrations of 7.3 and 14.25 µg/ml (p<0.01). Although the expressions of MCP-1, LOX-1, and eNOS mRNA were decreased at certain concentrations of Se-NPs (p<0.01 and p<0.05, respectively) in the treated bone marrow-derived EPCs, no significant differences were observed in the VCAM-1 mRNA expression levels in bone marrow-derived EPCs compared with the control group (P>0.05). Conclusions: This was the first report to demonstrate the effects of Se-NPs on proliferative, anti-oxidative, and anti-inflammatory activities for bone marrow-derived EPCs and blood-derived EPCs. Our findings suggested that Se-NPs could be considered as an effective agent that may ameliorate vascular problems.

Low Levels of Circulating EPCs Following Bone Marrow Carcinogenic Stimulus Predict the Onset of Hematological Tumors.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4258-4258
Author(s):  
Rita Fragoso ◽  
Catia Igreja ◽  
Manuela Ferreira ◽  
Sergio Dias
Keyword(s):  
Bone Marrow ◽  
Acute Leukemia ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Whole Body ◽  
Control Group ◽  
Disease Group ◽  
Early Disease ◽  
Endothelial Progenitor ◽  
Low Levels

Abstract Endothelial progenitor cells (EPCs) originate in the bone marrow (BM), proliferate, migrate and differentiate into endothelial cells, contributing to the formation of new blood vessels in normalcy and in malignant tumor growth. EPCs have been detected at increased frequency in the circulation of cancer patients and lymphoma-bearing mice, and tumor VEGF production correlates with EPCs mobilization. In order to clarify the contribution and importance of endothelial progenitor cells during tumor development, we established a murine carcinogenesis model that produces hematological neoplasias, namely thymomas and acute leukemia. This model consisted of administering 3 cycles of irradiation (sub-lethally), within one month of interval between them. Every month after the last irradiation, the levels of circulating endothelial progenitor cells (Flk-1+ and Sca+ cells) and hematopoietic progenitor cells (FLT-1+ and Sca+ cells) in peripheral blood were quantified (by flow cytometry). A first assay was done using 30 mice (FVB/N strain), divided into 2 groups: the control group (not irradiated) with 10 mice and the irradiated group with 20 mice. At the end of the assay (~11 months after last irradiation) the incidence of tumors was approximately 63% in the irradiated group (of these, there was an equal incidence of thymomas and acute leukemia). About 37% of the irradiated mice presented signs of disease 2,5 moths after the last irradiation ( called early disease group) while the other 26% presented signs of disease 7,2 months after the last irradiation ( called late disease group). Surprisingly, when comparing the EPC levels between the two groups that developed tumors and the remaining irradiated mice that did not (called no disease group), the two groups of mice that developed tumors had a decreased number of circulating EPC. This decreased was more evident in the early disease group (p&lt;0.01). An inverse relation was observed for VEGF levels in circulation, since the mice with no disease presented lower VEGF levels (5pg/ml) comparied with the two groups that developed tumors (&gt;10pg/ml). At this point, we hypothesized the BM derived EPC levels somehow modulated the onset of hematological disease in irradiated mice. To modulate EPC levels, we transplanted EPCs into irradiated mice with low levels of circulating EPCs. In a preliminary experiment, mice (n=2) that received exogenous EPCs survived, while the mice that did not succumbed to hematological diseases. Taken together, the data obtained suggest a role for EPCs in modulating the BM microenvironment, thus regulating the onset of hematological malignancies. Ongoing studies are addressing possibility. Finally, these results suggest that detection of reduced circulating BM EPCs levels following cyclic whole body irradiation may predict a worse disease outcome.

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