Brief Review |
From the Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, the Netherlands.
Correspondence to Prof Dr Adriana C. Gittenberger-de Groot, Department of Anatomy and Embryology, PO Box 9602, 2300RC Leiden, the Netherlands. E-mail acgitten@mail.medfac.leidenuniv.nl
| Introduction |
|---|
If we focus on the development of intimal thickening in the latter function, it is clear that even this pathological subset presents itself in various forms. That is, arteriosclerosis after hypertension,1 atherosclerosis,2 and restenosis after percutaneous transluminal coronary angioplasty or coronary artery bypass grafting surgery3 have features in common as well as characteristics selective for each disease.
Relevant to an understanding of the above processes is the basic question of whether we are dealing either with a SMC heterogeneity in origin or with a spatiotemporal heterogeneity in expression of differentiation markers. To add to this complexity there is an increasing evidence that already committed and differentiated cells can transdifferentiate into another cell type. In studying SMC heterogeneity, a combination of these factors is likely.
It has been shown by several research groups that SMC heterogeneity exists within the vessel wall, varying from the adult rat4 5 to the human fetal population.6 These data are mainly based on in vitro cell culture studies.
A different approach is to study the intact vascular wall and
expression of differentiation markers.7 8 9 10 11 This approach
shows a change in gene expression patterns with normal maturation and
with development of intimal thickening of the vessel wall. During
development of intimal thickening in various settings, including
physiological circumstances,11
thickening experimentally induced by a
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