Copyright © 2006, European Society of Cardiology
Do intrinsic arterial wall features determine atherosclerosis susceptibility?
aDepartment of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, The Netherlands
bDepartment of Biomedical Technology, Eindhoven Institute of Technology, Eindhoven, The Netherlands
* Corresponding author. Department of Physiology, Maastricht University, 6229 ER Maastricht, The Netherlands. Tel.: +31 43 3881200; fax: +31 43 3884166. Email address: m.post{at}fys.unimaas.nl
Received 14 July 2006; accepted 18 July 2006
See article by Mahadevan et al. [5] (pages 60–68) in this issue.
It is generally accepted that the propensity of arteries to develop atherosclerotic lesions differs between arterial segments [1–4]. Within this context the carotid and coronary arteries are well known for their high susceptibility to develop atherosclerosis, whereas the internal mammary artery (IMA) is resistant. The underlying biology of this vascular susceptibility is still not completely elucidated and might be of great importance for our understanding of vascular cues that will protect against atherosclerosis.
One set of such cues might be intrinsic as exemplified by the study of Mahadevan et al. in this issue of Cardiovascular Research [5]. They show characteristic differences for smooth muscle cells (SMCs) derived from either internal mammary or coronary arteries in cell migration towards oxidized lipoproteins (ox-LDL), antioxidant capacity, and NOS activation [5]. The high anti-oxidant capacity of the IMA compared to coronary artery SMCs is especially relevant as it might block ox-LDL-induced chemotaxis and potentially lowers atherosclerotic susceptibility. Reactive oxygen species (ROS) are involved in a plethora of important signalling cascades within vascular cells (e.g. signalling via VEGF, NO, and PDGF) and are under critical control of antioxidant systems (e.g. Mn,Zn-superoxide dismutase, peroxiredoxins, and glutathione peroxidase) [6,7]. Intracellular ROS imbalance can result in disturbed vascular function as demonstrated by the authors for ox-LDL- and angiotensin II-induced SMC chemotaxis [5]. Reduced migratory capacity of IMA-derived SMCs has been consistently reported by others [2], although the majority of these studies compared the IMA with the saphenous vein and the radial artery.
The data of the study of Mahadevan and colleagues add considerably to the growing knowledge on vascular heterogeneity and susceptibility to atherogenesis. Particularly in the IMA, wall structure and biochemical composition have been related to the resistance against atherosclerosis [2,3,5]. Other characteristics of IMA-derived SMCs that have been highlighted include, but are not limited to, reduced proliferation and increased apoptosis rates [3] and lower expression (as compared to coronary SMCs) of decorin and tenascin, which are functionally linked to LDL binding and SMC migration [4]. This difference in characteristics and functional heterogeneity might be SMC lineage dependent [1]. SMCs populating the IMA are mesenchymal (i.e. mesodermal origin) derived, whereas the carotid artery and aorta are mainly neural crest cell (NCC; i.e. ectomesodermal origin) related [8]. In contrast, the coronary artery SMCs are predominantly recruited from a special epithelial mesothelium [9] and NCC-derived SMCs are found in the proximal part of the coronary artery system [8]. Interestingly, a markedly reduced antioxidant capacity (i.e. catalase) has been described for the NCCs [10] that might lead to a higher susceptibility to ox-LDL and, likely, the tendency of the coronary system and carotid artery to develop atherosclerotic lesions. Due to the heterogeneity in the origin of coronary SMCs it remains uncertain what kind of coronary SMCs were used by Mahadevan and colleagues. It should also be noted that within the IMA, heterogeneity of SMC phenotypes exists [11] that could relate to transition from an elastic towards a muscular wall architecture for the proximal to distal part of the IMA, respectively. Extrinsic cues such as shear stress, axial stretch, and paucity of side branches might contribute to these local differences and could reflect a distinct atherosclerotic susceptibility as well.
The IMA is not completely immune to atherogenic influences [12] as demonstrated by the presence of early features of atherosclerosis in patients with advanced atherosclerosis, including medionecrosis and enhanced endothelin production and endothelin receptor expression [13]. Also, in experimental studies, the IMA can respond to a high cholesterol diet by inducing angiogenesis of the vasa vasorum, which has been interpreted as an early atherogenic response [14]. When placed in a coronary position, intimal hyperplasia and atherosclerosis in the IMA is still not prominent, suggesting that some level of protection persists after grafting. Although IMA has been used as an in vitro model of arterial response to stenting, no comparison was made with other in vitro models. Thus, it is unknown how IMA-derived SMCs respond to vascular injury, for instance after stenting. Therefore, the pathophysiologic relevance of the observed differences in SMC migration by Mahadevan and colleagues warrants further attention.
Judged by the relative patency rates that are emerging for alternative arterial grafts [15], it seems likely that whatever protects the IMA from atherosclerosis in situ or as a graft may be shared to some extent by arteries such as the radial, gastroepiploic, and inferior epigastric arteries. It would therefore be reasonable and helpful to extend studies like the one performed by Mahadevan et al. with predilection sites of atherosclerosis in direct comparison with protected areas in the vascular tree. Additional experiments are required to solve the emerging question of whether intrinsic vascular wall features determine the susceptibility to develop atherosclerosis. Within this area of research a clear distinction between endothelium and SMC function and dysfunction as well as their interaction will be of elementary importance.
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