scholarly journals The bone marrow–cardiac axis: role of endothelial progenitor cells in heart failure☆

2011 ◽  
Vol 39 (3) ◽  
pp. 368-374 ◽  
Author(s):  
Simon Maltais ◽  
Louis P. Perrault ◽  
Hung Q. Ly
Keyword(s):  
Heart Failure ◽  
Bone Marrow ◽  
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.

Potential role of endothelial progenitor cells in the pathophysiology of heart failure: Clinical implications and perspectives

2006 ◽  
Vol 189 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Ioannis Andreou ◽  
Dimitris Tousoulis ◽  
Costas Tentolouris ◽  
Charalambos Antoniades ◽  
Christodoulos Stefanadis
Keyword(s):  
Heart Failure ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Potential Role ◽  
Clinical Implications ◽  
Endothelial Progenitor

scholarly journals Endothelial Progenitor Cells: An Appraisal of Relevant Data from Bench to Bedside

2021 ◽  
Vol 22 (23) ◽  
pp. 12874
Author(s):  
Doralisa Morrone ◽  
Maria Elena Lucia Picoi ◽  
Francesca Felice ◽  
Andrea De Martino ◽  
Cristian Scatena ◽  
...  
Keyword(s):  
Heart Failure ◽  
Bone Marrow ◽  
Acute Coronary Syndrome ◽  
Progenitor Cells ◽  
Endothelial Progenitor Cells ◽  
Clinical Settings ◽  
Peripheral Vascular ◽  
Endothelial Progenitor ◽  
Great Opportunity ◽  
Coronary Syndrome

The mobilization of endothelial progenitor cells (EPCs) into circulation from bone marrow is well known to be present in several clinical settings, including acute coronary syndrome, heart failure, diabetes and peripheral vascular disease. The aim of this review was to explore the current literature focusing on the great opportunity that EPCs can have in terms of regenerative medicine.

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

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.

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