Translational control of JunB, an AP-1 transcription factor, in activated human endothelial cells

Abstract

Stimulated endothelial cells (EC) assume an activated phenotype with pro-inflammatory and prothrombotic features, requiring new gene and protein expression. New protein synthesis in activated EC is largely regulated by transcriptional events controlled by a variety of transcription factors. However, post-transcriptional control of gene expression also influences phenotype and allows the cell to alter protein expression in a faster and more direct way than is typically possible with transcriptional mechanisms. We sought to demonstrate that post-transcriptional control of gene expression occurs during EC activation. Using thrombin-activated EC and a high-throughput, microarray-based approach, we identified a number of gene products that may be regulated through post-transcriptional mechanisms, including the AP-1 transcription factor JunB. Using polysome profiling, cytoplasts and other standard cell biologic techniques, JunB is shown to be regulated at a post-transcriptional level during EC activation. In activated EC, the AP-1 transcription factor JunB, is regulated on a post-transcriptional level. Signal-dependent control of translation may regulate transcription factor expression and therefore, subsequent transcriptional events in stimulated EC.