Mutations and altered expression of specific genes have been shown to be responsible for a number of cardiovascular disorders, including chronic hypertension, coronary heart disease, stroke, and rheumatic heart disease as well as arrhythmias, congenital defects and diseases of the vessel wall. For many of these disorders, changes in gene expression leads to deleterious alterations of protein concentrations that may be compensated by therapeutic treatment. Identification of such changes in disease states may thus help indicate treatment strategies to prevent the disease or diminish its severity. An important tool for determining the impact of altered expression of selected genes is the genetically manipulated animal model, in which one or more genes are knocked out or knocked in. A relatively recent interest of our group has been to evaluate alterations in gene expression in various tissues of mice, in which the coding region of particular gap junction proteins (connexins) is disrupted by homologous recombination and in cultures of connexin-deficient cell lines transiently or stably transfected with connexins.
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