3P-0624 Role of bone marrow-derived progenitor cells in cuff-induced vascular injury in mice

2003 ◽  
Vol 4 (2) ◽  
pp. 199
Author(s):  
Y. Xu ◽  
H. Arai ◽  
H. Sano ◽  
M. Yoshimoto ◽  
S. Nishikawa ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Vascular Injury

scholarly journals Role of Bone Marrow–Derived Progenitor Cells in Cuff-Induced Vascular Injury in Mice

2004 ◽  
Vol 24 (3) ◽  
pp. 477-482 ◽  
Author(s):  
Yang Xu ◽  
Hidenori Arai ◽  
Xin Zhuge ◽  
Hideto Sano ◽  
Toshinori Murayama ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Vascular Injury

Abstract 11664: The Identification and Hierarchy of Bone Marrow-Derived Artery-Resident Mesodermal Progenitor Cells and Their Dynamics in Atherosclerosis

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Hyun-Jai Cho ◽  
Hyun-Ju Cho ◽  
Yoo-Wook Kwon ◽  
Young-Bae Park ◽  
Hyo-Soo Kim
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Peripheral Circulation ◽  
Humoral Factors ◽  
Cell Property ◽  
Apoe Ko Mice ◽  
Multiplex Cytokine ◽  
Developmental Hierarchy

Background: We recently identified bone marrow (BM)-derived artery resident calcifying progenitor cells. Sca-1+PDGFRα- cells may possess bipotent (osteoblastic/osteoclastic) characteristics. However, the nature of progenitor cells remains elusive. Hypothesis: We investigated developmental hierarchy of progenitor cells and in vivo dynamics in atherosclerosis. Methods and Results: We harvested cells from BM and artery of C57 mice. In BM, Lin-CD29+Sca-1+PDGFRα- cells showed hematopoietic potential and differentiated into osteoclasts (OC). They also possessed mesenchymal stem cell property including osteoblastic (OB) differentiation, suggesting that Sca-1+PDGFRα- cells could be mesodermal progenitor cells. Interestingly, BM-derived artery-resident, clonal Sca-1+PDGFRα- cells maintained bipotency but lost hematopoietic nature. In contrast, Sca-1+PDGFRα+ cells in BM and artery only showed unipotency (OB). When we overexpressed or knocked down PDGFRα, there was no alteration in OB or OC differentiation of Sca-1+PDGFRα- cells and no effect on OB differentiation of Sca-1+PDGFRα+ cells, indicating PDGFRα as a surface marker but not a functional player. In hyperlipidemic ApoE-KO mice compared with control, Sca-1+PDGFRα- cells were less mobilized from BM to peripheral circulation and less infiltrated into atherosclerotic plaque, whereas Sca-1+PDGFRα+ cells were not significantly affected. Multiplex cytokine assay of serum and artery revealed that IL-1β was significantly increased and IL-5 was markedly decreased in atherosclerotic mice. IL-1β decreased the migration of Sca-1+PDGFRα- cells by 5 folds compared with TNFα, and IL-5 increased the migration as much as TNFα. But the migration of Sca-1+PDGFRα+ cells was not altered. These data indicate that atherosclerosis-related humoral factors mainly regulated mesodermal progenitor cells’ dynamics. Conclusion: We demonstrate that Sca-1+PDGFRα- cell is a mesodermal progenitor cell that possesses both hematopoietic and mesenchymal potentials. In atherogenesis, the mobilization and infiltration of Sca-1+PDGFRα- progenitor cells were regulated by IL-1β and IL-5. These data provide a novel mechanism regarding the role of bipotent progenitor cells in atherosclerosis.

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.

Abstract P034: Bone Marrow--Derived Cells Are Not an Essential Component in Cardiosphere Formation

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Jianqin Ye ◽  
Andrew Boyle ◽  
Yerem Yeghiazarians
Keyword(s):  
Myocardial Infarction ◽  
Bone Marrow ◽  
Progenitor Cells ◽  
Small Cells ◽  
Immunomagnetic Beads ◽  
Cell Component ◽  
Post Surgery ◽  
C57bl Mice ◽  
Bone Marrow Derived Cells

Background: Cardiospheres (CS) are composed of heterogeneous population of cells but it is unknown whether bone marrow derived cells are an essential cell component in CS formation. Methods: Chimera mice were generated by transplantation of bone morrow cells from GFP transgenic mice to irradiated C57BL mice. Mice were randomized into 3 groups 5 months after transplantation: 1) myocardial infarction; 2) sham operated; 3) un-operated (n=5/group). Hearts were harvested 2-weeks post-surgery. Cardiac explants were cultured and putative cardiosphere forming cells (CFCs) (small cells migrating out from the explants) were collected 14 days later and reseeded on new culture dishes for CS formation. The number of CS from each heart was counted at 3 days. CS cell composition was analyzed by FACS. To further analyze the role of bone marrow derived CD45+ cells in forming CS, CD45+ cells was isolated from CFCs by CD45 antibody coated immunomagnetic beads. The number of CS formed from 1×10 5 putative CFCs, CFCs without CD45+ cells and CD45+ cells from CFCs (n=6-9/cell type) respectively were also counted at 3 days in culture. Results: Compared to sham (122± 23/heart) and un-operated hearts (18± 5/heart), infarcted hearts formed more CS (357± 64/heart, P<0.01). In all groups, irrespective of any surgery, 18.4± 4.5% of cells in CS co-expressed GFP and CD45, indicating they originated in bone marrow. Low percentage of bone marrow stem/progenitor cells (3.9% Sca-1+GFP+CD45+ and 1% c-Kit+GFP+CD45+ cells) were detected in CS, but a high percentage of cells within CS were cardiac stem/progenitor cells (26.3± 9.4% cells were Sca-1+GFP-CD45-, 0.10± 0.04% c-Kit+GFP-CD45-). Depleting CD45+ cells from putative CFCs actually increased the formation of CS (67±10 CS/1×10 5 cells) compared to un-depleted CFCs (51± 6 CS/1×10 5 cells, P<0.0001). Purified CD45+ cells from CFCs did not form CS in culture. Conclusion: Myocardial infarction increases the formation of CS in culture. Bone marrow derived CD45+ cells make up a small percentage of CS, but are not necessary for CS formation.

scholarly journals Activation of heme oxygenase-1 by Ginkgo biloba extract differentially modulates endothelial and smooth muscle-like progenitor cells for vascular repair

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tao-Cheng Wu ◽  
Jia-Shiong Chen ◽  
Chao-Hung Wang ◽  
Po-Hsun Huang ◽  
Feng-Yen Lin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Smooth Muscle ◽  
Progenitor Cells ◽  
Heme Oxygenase ◽  
Neointimal Hyperplasia ◽  
Vascular Repair ◽  
Vascular Progenitor Cells

AbstractVascular progenitors such as endothelial progenitor cells (EPCs) and smooth muscle-like progenitor cells (SMPCs) may play different roles in vascular repair. Ginkgo biloba extract (GBE) is an exogenous activator of heme oxygenase (HO)-1, which has been suggested to improve vascular repair; however, the detailed mechanisms have yet to be elucidated. This study aimed to investigate whether GBE can modulate different vascular progenitor cells by activating HO-1 for vascular repair. A bone marrow transplantation mouse model was used to evaluate the in vivo effects of GBE treatment on wire-injury induced neointimal hyperplasia, which is representative of impaired vascular repair. On day 14 of GBE treatment, the mice were subjected to wire injury of the femoral artery to identify vascular reendothelialization. Compared to the mice without treatment, neointimal hyperplasia was reduced in the mice that received GBE treatment for 28 days in a dose-dependent manner. Furthermore, GBE treatment increased bone marrow-derived EPCs, accelerated endothelial recovery, and reduced the number of SMPCs attached to vascular injury sites. The effects of GBE treatment on neointimal hyperplasia could be abolished by co-treatment with zinc protoporphyrin IX, an HO-1 inhibitor, suggesting the in vivo role of HO-1. In this in vitro study, treatment with GBE activated human early and late EPCs and suppressed SMPC migration. These effects were abolished by HO-1 siRNA and an HO-1 inhibitor. Furthermore, GBE induced the expression of HO-1 by activating PI3K/Akt/eNOS signaling in human late EPCs and via p38 pathways in SMPCs, suggesting that GBE can induce HO-1 in vitro through different molecular mechanisms in different vascular progenitor cells. Accordingly, GBE could activate early and late EPCs, suppress the migration of SMPCs, and improve in vivo vascular repair after mechanical injury by activating HO-1, suggesting the potential role of pharmacological HO-1 activators, such as GBE, for vascular protection in atherosclerotic diseases.

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