The Experts below are selected from a list of 30780 Experts worldwide ranked by ideXlab platform
Wang Zhenh - One of the best experts on this subject based on the ideXlab platform.
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Soluble epoxide hydrolase inhibitors on the migration function of Endothelial Progenitor Cell
Fujian Medical Journal, 2014Co-Authors: Wang ZhenhAbstract:Objective To study the effect of different concentration of soluble epoxide hydrolase inhibitor t-AUCB on the migration function of Endothelial Progenitor Cell.Methods Density gradient centrifugation was applied to separate and obtain mouse bone marrow Progenitor Cells,pre-intervention of Endothelial Progenitor Cells was carried out with different concentrations of t-AUCB,and theEPCs migration ability after the intervention in vitro was detected.Results From 0-100μmol/L,as the concentration increased,t-AUCB could increase EPCs migration ability with concentration dependence in vitro.ConclusionSoluble epoxide hydrolase inhibitor t-AUCB participates in positive regulation on the migration function of EPCs.
Willem J. Giessen - One of the best experts on this subject based on the ideXlab platform.
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the genous Endothelial Progenitor Cell capture stent accelerates stent re Endothelialization but does not affect intimal hyperplasia in porcine coronary arteries
Catheterization and Cardiovascular Interventions, 2012Co-Authors: Heleen M M Van Beusekom, Oana Sorop, Gökhan Ertaş, Willem J. GiessenAbstract:Objectives: To study the effect of Endothelial Progenitor Cell (EPC) capture on the vascular response to coronary stenting. Background: The introduction of drug-eluting stents has reduced the need for target lesion revascularization, but their effect on delayed healing, inflammation, and vascular dysfunction has emphasized the need to design strategies that improve current DES. One such strategy is to improve Endothelialization by capturing CD34-positive Cells (EPC) by the stent surface. The first human clinical trial using coronary EPC capture stents showed stent safety but neointimal thickness (NIT) was not reduced compared to bare metal stents (BMS). To understand these responses we studied the coronary response to the EPC capture stent in swine. Methods and Results: The stent, coated with murine antihuman monoclonal CD34 antibodies, was assessed with QCA guided stent implantation in normal swine coronary arteries for early Endothelialization at 2 and 5 days, and NIT at 28 and 90 days in comparison to control stents carrying a non-specific murine antibody or to BMS. The main finding was that while the EPC capture stent significantly improved early Endothelialization it did not reduce NIT at 28 and 90 days. Conclusions: The EPC capture stent improves early Endothelialization in swine but this does not affect neointimal thickness as compared to control stents at 28 and 90 days. © 2011 Wiley Periodicals, Inc.
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the genous Endothelial Progenitor Cell capture stent accelerates stent re Endothelialization but does not affect intimal hyperplasia in porcine coronary arteries
Catheterization and Cardiovascular Interventions, 2012Co-Authors: Heleen M M Van Beusekom, Oana Sorop, Gökhan Ertaş, Willem J. GiessenAbstract:OBJECTIVES: To study the effect of Endothelial Progenitor Cell (EPC) capture on the vascular response to coronary stenting. BACKGROUND: The introduction of drug-eluting stents has reduced the need for target lesion revascularization, but their effect on delayed healing, inflammation, and vascular dysfunction has emphasized the need to design strategies that improve current DES. One such strategy is to improve Endothelialization by capturing CD34-positive Cells (EPC) by the stent surface. The first human clinical trial using coronary EPC capture stents showed stent safety but neointimal thickness (NIT) was not reduced compared to bare metal stents (BMS). To understand these responses we studied the coronary response to the EPC capture stent in swine. METHODS AND RESULTS: The stent, coated with murine antihuman monoclonal CD34 antibodies, was assessed with QCA guided stent implantation in normal swine coronary arteries for early Endothelialization at 2 and 5 days, and NIT at 28 and 90 days in comparison to control stents carrying a non-specific murine antibody or to BMS. The main finding was that while the EPC capture stent significantly improved early Endothelialization it did not reduce NIT at 28 and 90 days. CONCLUSIONS: The EPC capture stent improves early Endothelialization in swine but this does not affect neointimal thickness as compared to control stents at 28 and 90 days.
Takehisa Matsuda - One of the best experts on this subject based on the ideXlab platform.
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fabrication of Endothelial Progenitor Cell epc seeded intravascular stent devices and in vitro Endothelialization on hybrid vascular tissue
Biomaterials, 2003Co-Authors: Toshihiko Shirota, Hisataka Yasui, Hiroaki Shimokawa, Takehisa MatsudaAbstract:Abstract Rapid re-Endothelialization at an atherosclerotic lesion after balloon inflation or stent deployment may be essential for reducing or preventing local thrombus formation and restenosis. In order to prevent these complications via enhanced rapid re-Endothelialization, we fabricated two types of Endothelial Progenitor Cell (EPC)-seeded intravascular stent devices. One was a photocured gelatin-coated metallic stent, and the other was a microporous thin segmented polyurethane (SPU) film-covered stent on which photocured gelatin was coated. Both devices were seeded with ex vivo expanded EPCs obtained from canine peripheral blood. Seeded EPCs formed confluent monolayers onto surfaces of both photocured gelatin-coated stent struts and SPU film, and a majority of Cells remained on surfaces of stents after stent expansion. The EPC-seeded stent was expanded in a tubular hybrid vascular medial tissue composed of vascular smooth muscle Cells and collagen as an arterial media mimic. After 7-day culture, EPCs, which migrated from the stent struts, proliferated and Endothelialized the luminal surfaces of the hybrid vascular medial tissue. This in vitro pilot study prior to in vivo experiments suggests that on-stent Cell delivery of EPCs may be novel therapeutic devices for re-Endothelialization or endothelium lining or paving at an atherosclerotic arterial wall, resulting in the prevention of on-stent thrombus formation and in-stent restenosis, as well as the rapid formation of normal tissue architecture.
Heleen M M Van Beusekom - One of the best experts on this subject based on the ideXlab platform.
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the genous Endothelial Progenitor Cell capture stent accelerates stent re Endothelialization but does not affect intimal hyperplasia in porcine coronary arteries
Catheterization and Cardiovascular Interventions, 2012Co-Authors: Heleen M M Van Beusekom, Oana Sorop, Gökhan Ertaş, Willem J. GiessenAbstract:Objectives: To study the effect of Endothelial Progenitor Cell (EPC) capture on the vascular response to coronary stenting. Background: The introduction of drug-eluting stents has reduced the need for target lesion revascularization, but their effect on delayed healing, inflammation, and vascular dysfunction has emphasized the need to design strategies that improve current DES. One such strategy is to improve Endothelialization by capturing CD34-positive Cells (EPC) by the stent surface. The first human clinical trial using coronary EPC capture stents showed stent safety but neointimal thickness (NIT) was not reduced compared to bare metal stents (BMS). To understand these responses we studied the coronary response to the EPC capture stent in swine. Methods and Results: The stent, coated with murine antihuman monoclonal CD34 antibodies, was assessed with QCA guided stent implantation in normal swine coronary arteries for early Endothelialization at 2 and 5 days, and NIT at 28 and 90 days in comparison to control stents carrying a non-specific murine antibody or to BMS. The main finding was that while the EPC capture stent significantly improved early Endothelialization it did not reduce NIT at 28 and 90 days. Conclusions: The EPC capture stent improves early Endothelialization in swine but this does not affect neointimal thickness as compared to control stents at 28 and 90 days. © 2011 Wiley Periodicals, Inc.
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the genous Endothelial Progenitor Cell capture stent accelerates stent re Endothelialization but does not affect intimal hyperplasia in porcine coronary arteries
Catheterization and Cardiovascular Interventions, 2012Co-Authors: Heleen M M Van Beusekom, Oana Sorop, Gökhan Ertaş, Willem J. GiessenAbstract:OBJECTIVES: To study the effect of Endothelial Progenitor Cell (EPC) capture on the vascular response to coronary stenting. BACKGROUND: The introduction of drug-eluting stents has reduced the need for target lesion revascularization, but their effect on delayed healing, inflammation, and vascular dysfunction has emphasized the need to design strategies that improve current DES. One such strategy is to improve Endothelialization by capturing CD34-positive Cells (EPC) by the stent surface. The first human clinical trial using coronary EPC capture stents showed stent safety but neointimal thickness (NIT) was not reduced compared to bare metal stents (BMS). To understand these responses we studied the coronary response to the EPC capture stent in swine. METHODS AND RESULTS: The stent, coated with murine antihuman monoclonal CD34 antibodies, was assessed with QCA guided stent implantation in normal swine coronary arteries for early Endothelialization at 2 and 5 days, and NIT at 28 and 90 days in comparison to control stents carrying a non-specific murine antibody or to BMS. The main finding was that while the EPC capture stent significantly improved early Endothelialization it did not reduce NIT at 28 and 90 days. CONCLUSIONS: The EPC capture stent improves early Endothelialization in swine but this does not affect neointimal thickness as compared to control stents at 28 and 90 days.
Guo-yuan Yang - One of the best experts on this subject based on the ideXlab platform.
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Adiponectin modulates the function of Endothelial Progenitor Cells via AMPK/eNOS signaling pathway.
Biochemical and biophysical research communications, 2017Co-Authors: Shuhong Wang, Jie Miao, Guo-yuan Yang, Linhui ShenAbstract:Endothelial Progenitor Cells have been shown to differentiate into Endothelial Cells and to play a pivotal role in vascular homeostasis. Adiponectin has anti-atherogenic and anti-inflammatory properties via directly acting on vascular Cells. The aim of the present study is to explore the effect of adiponectin on major functions involved in survival, migration, and tube formation of Endothelial Progenitor Cells and to explore the underlying mechanism. In this study, we transferred adiponectin gene into Endothelial Progenitor Cells via lentiviral vectors and investigated the proliferation, migration and tube formation of these transfected Cells. We found that adiponectin is highly expressed in Endothelial Progenitor Cells and promotes their proliferation, migration and tube formation. Western blot data showed that the former two processes were mediated through the AMPK/Akt/eNOS pathway, the latter via the AMPK/eNOS pathway. Use of the AMPK inhibitor (Compound C) or Akt inhibitor (MK-2206) reduced eNOS phosphorylation and attenuated adiponectin-induced Endothelial Progenitor Cell proliferation, migration and tube formation compared to the controls (p < 0.05). Taken together, these data indicated that adiponectin promotes Endothelial Progenitor Cell proliferation and migration via AMPK/Akt/eNOS signaling pathway and promotes tube formation through AMPK/eNOS, suggesting that adiponectin-transduced Endothelial Progenitor Cell transplantation is a potential therapeutic target for vascular disease.
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Endothelial Progenitor Cell transplantation improves long term stroke outcome in mice
Annals of Neurology, 2010Co-Authors: Yongfeng Fan, Fanxia Shen, Tim Frenzel, Wei Zhu, Jianrong Liu, Yongmei Chen, William L Young, Guo-yuan YangAbstract:Endothelial Progenitor Cells (EPCs) have been implicated in playing an important role in vascular repair and revascularization in ischemic organs including brain tissue. However, the cause of EPC migration and the function of EPC playing following post-ischemia are unclear. Here, we reported EPC therapy in a mouse model of transient middle cerebral artery occlusion (tMCAO) to explore the roles of EPC following ischemic brain injury. Human EPCs were cultured, characterized, and confirmed with flow cytometry. Ex vivo expanded EPCs (1×106) were injected via jugular vein after 1 hour of tMCAO. Histological and behavioral analyses were performed from day 1 to 28 days after tMCAO. EPCs were detected in ischemic brain region 24 hours after MCAO. EPC transplantation significantly reduced ischemic infarct volume at 3 days following MCAO compared to the control (p<0.05). CXCR4 was expressed on majority of EPCs and SDF-1-induced EPC migration was blocked by AMD3100 in vitro. SDF-1 was up-regulated in ischemic brain and AMD3100 could reduce EPCs migration to the ischemic region in vivo, suggesting that SDF-1/CXCR4 was involved in EPC-mediated neuroprotection. Compared to the control, EPC therapy reduced mouse cortex atrophy 4 weeks after tMCAO, which was accompanied by improved neurobehavioral outcomes (p<0.05). In addition, EPC injection potently increased angiogenesis in the peri-infarction area (p<0.05). We conclude that systemic delivery of EPC protect against cerebral ischemic injury, promote neurovascular repair, and improve long-term neurobehavioral outcomes. Our data suggests that SDF-1/CXCR4 plays a critical role in EPC-mediated neuroprotection.
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interleukin 6 stimulates circulating blood derived Endothelial Progenitor Cell angiogenesis in vitro
Journal of Cerebral Blood Flow and Metabolism, 2008Co-Authors: Yongfeng Fan, Fanxia Shen, Wei Zhu, Yongmei Chen, William L Young, Yiqian Zhu, Yerem Yeghiazarians, Michael T Lawton, Guo-yuan YangAbstract:Circulating blood Endothelial Progenitor Cells (EPCs) contribute to postnatal vasculogenesis, providing a novel therapeutic target for vascular diseases. However, the molecular mechanism of EPC-induced vasculogenesis is unknown. Interleukin-6 plays multiple functions in angiogenesis and vascular remodeling. Our previous study demonstrated that the polymorphism (174G>C) in IL-6 gene promoter was associated with brain vascular disease. In this study, we investigated if IL-6 receptor is expressed in human EPCs derived from circulating mononuclear Cells, and if interleukin-6 (IL-6) stimulates EPC angiogenesis in vitro. First, we isolated and cultured mononuclear Cells from adult human circulating blood. We obtained EPC clones that were further cultured and expended for the angiogenesis study. We found that the EPCs possessed human mature Endothelial Cell phenotypes; however, they proliferated much faster than mature Endothelial Cells (P<0.05). We then found that IL-6 receptor (gp-80) was expressed in the EPCs, and that administration of IL-6 could activate receptor gp80/gp130 signaling pathways including downstream extraCellular signal-regulated kinase 1/2 and STAT3 phosphorylation in EPCs. Furthermore, IL-6 stimulated EPC proliferation, migration, and matrigel tube formation in a dose-dependent manner (P<0.05); anti-IL-6 antibodies or IL-6 receptor could abolish these effects (P<0.05). These results suggest that IL-6 plays a crucial role in the biologic behavior of blood-derived EPCs, which may help clarify the mechanism of IL-6 inflammatory-related diseases.