Genes, Matrix, and Restenosis
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One of the major advances in vascular biology over the last 2 decades has been the realization that the vessel wall is an active, integrated tissue composed of multiple distinct cell types coupled to one another by complex regulated interactions. Blood vessels are capable of sensing their milieu and integrating information from diverse stimuli, both humoral and biomechanical. In response to alterations in these signals, such as with mechanical injury or sustained hemodynamic changes, the vessel is capable of adapting itself, an effect known as vascular remodeling. This process can result in a spectrum of changes within the vessel wall, ranging from alterations in the cellular and extracellular (matrix) content of the wall to changes in the reactivity and functional properties of the vessel. The advent of techniques that allow more efficient discovery of the genes involved in these processes as well as a description of their temporal patterns of expression is now providing a powerful opportunity to begin to understand vascular remodeling at the molecular level.
There are now multiple approaches aimed at understanding the repertoire of gene expression in a given biological context. These range from techniques such as differential display1 and subtractive cloning strategies,2 which are designed to identify unknown genes whose expression is modulated under the conditions being examined, to transcriptional profiling strategies,3 in which a set of known sequences are prepared as an array and their patterns of expression are determined in parallel. In general, the latter have the advantage of allowing one to identify global patterns of gene expression for a defined cohort of genes, whereas the former allow for the discovery of new species that may not …