@entity723 and @entity39769 orphan receptor: two 'atheroprotective' genes as evidenced in dedicated XXXX models.

@entity1 @entity19 @entity3960 @entity723 @entity731 @entity39769
1. @entity731 is a multifactorial, inflammatory disease of the arterial vessel wall that is promoted by various well-defined risk factors. Although numerous genes, expressed in different vascular and inflammatory cells, have been implicated in this disease, it is widely appreciated that most of the genes and gene products vital for initiation and progression of @entity731 are unknown. 2. We follow two strategies in an attempt to make up for the void of essential knowledge. First, we study candidate genes that have not been implied in @entity1 @entity731 before, notably the differentiation factor @entity723 A. 3. Second, we performed a genome-wide search by differential display reverse transcription-polymerase chain reaction. This study indicated potential involvement of the @entity39769 orphan receptor transcription factor in @entity3960 ( @entity3960 ) (patho)physiology. 4. To reveal functional involvement of these proteins in @entity3960 during @entity731 , we performed experiments with @entity19 models, adjusted either to the characteristics of a secreted protein or to that of an intracellular transcription factor. 5. The secreted protein @entity723 A was studied in @entity19 infected systemically with recombinant adenoviral vehicles, resulting in predominant hepatic expression and subsequent high protein levels in the circulation. 6. To study the role of @entity39769 in @entity731 , we generated @entity19 in which promoter sequences were applied that direct expression of the transgenes to @entity3960 of the arterial tree. 7. Two approaches were taken to induce the formation of @entity3960 -rich lesions: (i) activation of femoral artery @entity3960 by placement of a loosely fitting cuff; and (ii) ligation of the carotid artery. 8. The aim of the present review is to illustrate the different approaches that can be taken to assess the potential relevance of genes in @entity731 in carefully selected @entity19 models. 9. Based on the results described, we propose that both @entity723 A and @entity39769 prevent excessive @entity3960 proliferation.
