The role of stem cells in vein graft remodelling

2007 ◽  
Vol 35 (5) ◽  
pp. 895-899 ◽  
Author(s):  
Q. Xu

The vessel wall is a dynamic tissue that undergoes positive remodelling in response to altered mechanical stress. A typical example is vein graft remodelling, because veins do not develop arteriosclerosis until a vein segment is grafted on to arteries. In this process, it was observed that vascular endothelial and smooth muscle cells of vein grafts die due to suddenly elevated blood pressure. This cell death is followed by endothelial regeneration. Central to this theme is the essential role played by EPCs (endothelial progenitor cells) in regenerating the lost endothelium. The mechanisms by which EPCs attach to the vessel wall and differentiate into mature endothelial cells involve increased chemokine production and laminar shear flow stimulation on the vessel wall. It seems that neo-endothelial cells derived from EPCs lack mature cell functions and express high levels of adhesion molecules resulting in LDL (low-density lipoprotein) penetration and mononuclear cell infiltration into the sub-endothelial space. Among infiltrated mononuclear cells, there are smooth muscle progenitors that proliferate and differentiate into smooth muscle cells. Meanwhile, stem cells present in the media and adventitia may also migrate into arteriosclerotic lesions via the vasa vasorum that are abundant in the diseased vessels. However, the molecular events leading to the homing, differentiation and maturation of stem/progenitor cells still needs elucidation. The present review attempts to update the progress in stem cell research related to the pathogenesis of vein graft arteriosclerosis or remodelling, focusing on the mechanisms by which stem/progenitor cells participate in the development of lesions, and to discuss the controversial issues and the future perspectives surrounding this research area.

1982 ◽  
Vol 48 (01) ◽  
pp. 101-103 ◽  
Author(s):  
B Kirchhof ◽  
J Grünwald

SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.


2011 ◽  
Vol 20 (3) ◽  
pp. e91-e94 ◽  
Author(s):  
Marc Jevon ◽  
Tahera I. Ansari ◽  
Jonathan Finch ◽  
Mustafa Zakkar ◽  
Paul C. Evans ◽  
...  

2006 ◽  
Vol 26 (12) ◽  
pp. 2696-2702 ◽  
Author(s):  
Jacob F. Bentzon ◽  
Charlotte Weile ◽  
Claus S. Sondergaard ◽  
Johnny Hindkjaer ◽  
Moustapha Kassem ◽  
...  

2013 ◽  
Vol 13 (02) ◽  
pp. 1350050 ◽  
Author(s):  
ZHI-QIANG YAN ◽  
YU-QING LI ◽  
BIN-BIN CHENG ◽  
QING-PING YAO ◽  
LI-ZHI GAO ◽  
...  

Differentiation of endothelial progenitor cells (EPCs) plays important roles in endothelial repair after vessel injury. Endothelial cells (ECs), vascular smooth muscle cells (VSMCs), and mechanical forces, including cyclic strain and shear stress, synergistically form the microenvironment of EPCs. However, the synergistic effect of cyclic strain, ECs, and VSMCs on the differentiation of EPCs remains unclear. In the present study, EPCs were indirectly co-cultured with stretched ECs or VSMCs that were subjected to 5%, 1.25-Hz cyclic strain by using FX-4000T Strain Unit. Then, Western blot and real-time PCR were used to examine expressions of EC marker, i.e., vascular cell adhesion molecule (VCAM), CD31, von Willebrand factor (vWF); VSMC markers, i.e., α-actin, Calponin, and SM22α; and signaling molecules, i.e., p-Akt and p-ERK. In static, co-cultured ECs increased expression of VCAM and phosphorylation of Akt and ERK in EPCs compared to that in EPCs cultured alone. In EPCs, co-cultured VSMCs decreased expressions of CD31 and vWF, but increased expressions of Calponin and SM22α. Stretched ECs reduced expressions of CD31 and vWF, enhanced Calponin and SM22α, and repressed phosphorylations of Akt and ERK in EPCs. Stretched VSMCs decreased CD31, increased Calponin and SM22α expressions, and repressed phosphorylation of Akt and ERK in EPCs. Our results suggest that ECs promoted EPC differentiation into ECs in static. VSMCs in static, as well as stretched ECs and stretched VSMCs, promoted EPC differentiation into VSMCs. Phosphorylation of Akt and ERK might be involved in EPC differentiation, mediated by the stretched ECs and VSMCs.


Author(s):  
Taby Ahsan ◽  
Adele M. Doyle ◽  
Garry P. Duffy ◽  
Frank Barry ◽  
Robert M. Nerem

Vascular applications in regenerative medicine include blood vessel substitutes and vasculogenesis in ischemic or engineered tissues. For these repair processes to be successful, there is a need for a stable supply of endothelial and smooth muscle cells. For blood vessel substitutes, the immediate goal is to enable blood flow, but vasoactivity is necessary for long term success. In engineered vessels, it is thought that endothelial cells will serve as an anti-thrombogenic lumenal layer, while smooth muscle cells contribute to vessel contractility. In other clinical applications, what is needed is not a vessel substitute but the promotion of new vessel formation (vasculogenesis). A simplified account of vasculogenesis is that endothelial cells assemble to form vessel-like structures that can then be stabilized by smooth muscle cells. Overall, the need for new vasculature to transfer oxygen and nutrients is important to reperfuse not only ischemic tissue in vivo, but also dense, structurally complex engineered tissue. The impact of these vascular therapies, however, is limited in part by the low yield and inadequate in vitro proliferation potential of primary endothelial and smooth muscle cells. Thus, there is a need to address the cell sourcing issue for vascular cell-based therapies, potentially using stem cells.


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