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
2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Dylan Z Liu ◽  
Yuqi Cui ◽  
Jason Z Liu ◽  
Lingjuan Liu ◽  
Xin Li ◽  
...  

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.


2006 ◽  
Vol 189 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Ioannis Andreou ◽  
Dimitris Tousoulis ◽  
Costas Tentolouris ◽  
Charalambos Antoniades ◽  
Christodoulos Stefanadis

2021 ◽  
Vol 22 (23) ◽  
pp. 12874
Author(s):  
Doralisa Morrone ◽  
Maria Elena Lucia Picoi ◽  
Francesca Felice ◽  
Andrea De Martino ◽  
Cristian Scatena ◽  
...  

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.


2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Zhongjian Cheng ◽  
Venkata NS Garikipati ◽  
Suresh K Verma ◽  
May Trungcao ◽  
Chunlin Wang ◽  
...  

2020 ◽  
Vol 21 (7) ◽  
pp. 2466 ◽  
Author(s):  
Yi-Chou Hou ◽  
Chien-Lin Lu ◽  
Cai-Mei Zheng ◽  
Wen-Chih Liu ◽  
Tzung-Hai Yen ◽  
...  

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.


Sign in / Sign up

Export Citation Format

Share Document