The role of eNOS in the migration and proliferation of bone-marrow derived endothelial progenitor cells and in vitro angiogenesis

2015 ◽  
Vol 39 (4) ◽  
pp. 484-490 ◽  
Author(s):  
Aizhen Lu ◽  
Libo Wang ◽  
Liling Qian
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
In Vitro Angiogenesis

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.

Abstract 272: Chronic Hyperlipidemia Alters the Population of Endothelial Progenitor Cells in Bone Marrow and Peripheral Circulation via Both ROS-dependent and Independent Mechanisms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Dylan Z Liu ◽  
Yuqi Cui ◽  
Jason Z Liu ◽  
Lingjuan Liu ◽  
Xin Li ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Ldl Receptor ◽  
Peripheral Circulation ◽  
Cell Number ◽  
Ros Production ◽  
Endothelial Progenitor ◽  
Ros Formation

Background/Aims: Bone marrow (BM)-derived endothelial progenitor cells (EPCs) make significant contribution to the function and integrity of vasculature. The number of EPCs is significantly decreased in hyperlipidemic patients. Reactive oxygen species (ROS) and oxidative stress were considered an important mechanism for the development of atherosclerosis in hyperlipidemia. The present study was to determine the role of ROS production in the changes of EPC population in chronic hyperlipidemia. Methods and Results: EPC numbers and ROS formation in BM and blood were determined in wild-type (WT) male C57BL/6 mice and hyperlipidemic LDL receptor knockout (LDLR-/-) mice with high fat diet for 4 months. Intracellular blood, extracellular BM and blood ROS production was significantly increased in hyperlipidemic LDLR-/- mice that was effectively blocked with N-acetylcysteine treatment. Hyperlipidemia produced complex changes in EPC populations in BM and blood. The c-Kit+/CD31+ cell number was significantly decreased in BM and blood, and the numbers of CD34+/CD133+ cells and Sca-1+/Flk-1+ cells were significantly decreased in blood without change in BM, which were not affected by inhibition of ROS production. Interestingly, blood CD34+/Flk-1+ cell number was significantly increased in hyperlipidemic mice that was prevented when ROS formation was inhibited. Conclusions: Chronic hyperlipidemia produced significant and complex changes in EPC populations in both BM and circulation through both ROS-dependent and ROS-independent mechanisms in mice.

Determine exogenous humanDDAH2gene function in rabbit bone marrow-derived endothelial progenitor cells in vitro

2017 ◽  
Vol 35 (2) ◽  
pp. 69-76
Author(s):  
Sara Shoeibi ◽  
Shabnam Mohammadi ◽  
Hamid Reza Sadeghnia ◽  
Elahe Mahdipour ◽  
Majid Ghayour-Mobarhan
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor ◽  
Rabbit Bone

scholarly journals A new method of culturing rat bone marrow endothelial progenitor cells in vitro

2020 ◽  
Vol 10 (5) ◽  
pp. 1270-1279
Author(s):  
Zhaohong Kong ◽  
Meixin Chen ◽  
Jian Jiang ◽  
Jiang Zhu ◽  
Yumin Liu
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
New Method ◽  
Endothelial Progenitor ◽  
Rat Bone

scholarly journals Role of β2-integrins for homing and neovascularization capacity of endothelial progenitor cells

2004 ◽  
Vol 201 (1) ◽  
pp. 63-72 ◽  
Author(s):  
Emmanouil Chavakis ◽  
Alexandra Aicher ◽  
Christopher Heeschen ◽  
Ken-ichiro Sasaki ◽  
Ralf Kaiser ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Ex Vivo ◽  
Limb Ischemia ◽  
Endothelial Progenitor ◽  
Cell Monolayers ◽  
Β2 Integrins

The mechanisms of homing of endothelial progenitor cells (EPCs) to sites of ischemia are unclear. Here, we demonstrate that ex vivo–expanded EPCs as well as murine hematopoietic Sca-1+/Lin− progenitor cells express β2-integrins, which mediate the adhesion of EPCs to endothelial cell monolayers and their chemokine-induced transendothelial migration in vitro. In a murine model of hind limb ischemia, Sca-1+/Lin− hematopoietic progenitor cells from β2-integrin–deficient mice are less capable of homing to sites of ischemia and of improving neovascularization. Preactivation of the β2-integrins expressed on EPCs by activating antibodies augments the EPC-induced neovascularization in vivo. These results provide evidence for a novel function of β2-integrins in postnatal vasculogenesis.

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