Abstract 460: Diabetes Impairs Reparative Property of Bone Marrow-derived Endothelial Progenitor Cells: Role of Mir-499-mediated Hydrogen Sulfide Deficiency

2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Zhongjian Cheng ◽  
Venkata NS Garikipati ◽  
Suresh K Verma ◽  
May Trungcao ◽  
Chunlin Wang ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Hydrogen Sulfide ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor

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.

scholarly journals e0326 Effects of hydrogen sulfide on proliferation of bone marrow derived endothelial progenitor cells in mice

Heart ◽  
2010 ◽  
Vol 96 (Suppl 3) ◽  
pp. A101-A101
Author(s):  
L. Wei ◽  
L. Ai-min ◽  
W. Hang ◽  
Z. Jin-kun ◽  
H. Lan
Keyword(s):  
Bone Marrow ◽  
Hydrogen Sulfide ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Endothelial Progenitor

scholarly journals The Role of Vitamin D in Modulating Mesenchymal Stem Cells and Endothelial Progenitor Cells for Vascular Calcification

2020 ◽  
Vol 21 (7) ◽  
pp. 2466 ◽  
Author(s):  
Yi-Chou Hou ◽  
Chien-Lin Lu ◽  
Cai-Mei Zheng ◽  
Wen-Chih Liu ◽  
Tzung-Hai Yen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Vitamin D ◽  
Mesenchymal Stem Cells ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Vascular Calcification ◽  
Osteoblastic Differentiation ◽  
Endothelial Progenitor

Vascular calcification, which involves the deposition of calcifying particles within the arterial wall, is mediated by atherosclerosis, vascular smooth muscle cell osteoblastic changes, adventitial mesenchymal stem cell osteoblastic differentiation, and insufficiency of the calcification inhibitors. Recent observations implied a role for mesenchymal stem cells and endothelial progenitor cells in vascular calcification. Mesenchymal stem cells reside in the bone marrow and the adventitial layer of arteries. Endothelial progenitor cells that originate from the bone marrow are an important mechanism for repairing injured endothelial cells. Mesenchymal stem cells may differentiate osteogenically by inflammation or by specific stimuli, which can activate calcification. However, the bioactive substances secreted from mesenchymal stem cells have been shown to mitigate vascular calcification by suppressing inflammation, bone morphogenetic protein 2, and the Wingless-INT signal. Vitamin D deficiency may contribute to vascular calcification. Vitamin D supplement has been used to modulate the osteoblastic differentiation of mesenchymal stem cells and to lessen vascular injury by stimulating adhesion and migration of endothelial progenitor cells. This narrative review clarifies the role of mesenchymal stem cells and the possible role of vitamin D in the mechanisms of vascular calcification.

Abstract 458: Critical Role of Bone Marrow Nox2-based NADPH Oxidase in Neovascularization in Response to Hindlimb Ischemia: Impact on Endothelial Progenitor Cells Function

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Norifumi Urao ◽  
Hyoe Inomata ◽  
Ha Won Kim ◽  
Ronald Mckinney ◽  
Mazooma Razvi ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Nadph Oxidase ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Critical Role ◽  
Border Zone ◽  
Hindlimb Ischemia ◽  
Endothelial Progenitor ◽  
Deficient Mice

Bone marrow (BM) is the major reservoir for endothelial progenitor cells (EPCs). Postnatal neovascularization involves not only angiogenesis but also mobilization of EPCs from BM and their recruitment to the ischemic sites. We demonstrated that reactive oxygen species (ROS) derived from Nox2-based NADPH oxidase play an important role in reparative angiogenesis induced by hindlimb ischemia. However, role of Nox2-derived ROS in BM and EPC function in postnatal neovascularization is unknown. Here we show that Nox2 is the most highly expressed Nox enzymes in mouse BM cells (BMCs) and EPCs. Hindlimb ischemia of mice significantly increases Nox2 mRNA expression (2.3-fold) and ROS production (7.2-fold) in BMCs at 3 days after surgery, which is associated with an increase in number of EPC-like c-kit+Flk-1+ cells in peripheral blood (3.9-fold). Nox2-deficient mice show impairment of ischemia-induced flow recovery (68% inhibition) and significant reduction of ROS levels in BM (98% decrease) and EPC mobilization, as assessed by EPC culture assay (76% decrease) and FACS analysis of c-kit+Flk-1+ cells (33% decrease). Transplantation of wild-type (WT)-BM into Nox2-deficient mice rescues the defective neovascularization. Conversely, WT mice transplanted with Nox2-deficient BM show significant decrease of flow recovery (41% decrease) and capillary density (24% decrease) compared to WT-BM transplanted control. Intravenous infusion of WT-BM-mononuclear cells (MNCs), but not Nox2-deficient MNCs, into WT mice at 1 day after hindlimb ischemia significantly promotes neovascularization (37% increase). Infusion of fluorescent dye-labeled WT- and Nox2-deficient BMCs reveals that homing capacity of Nox2-deficient BMCs in ischemic border zone is significantly reduced (52% decrease). In vitro, VEGF-induced EPC migration (48% decrease) and BMCs invasion (68% decrease) are significantly inhibited in Nox2-deficient cells. In conclusion, Nox2-derived ROS in BM play a critical role in mobilization, homing and angiogenic capacity of EPCs, thereby promoting revascularization of ischemic tissue. Thus, NADPH oxidase in BM and EPCs is potential therapeutic targets for ischemic cardiovascular diseases.

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