Transcriptional regulation of endothelial cell adhesion molecules: a dominant role for NF-kappa B.
A growing body of evidence demonstrates that elevated expression of the endothelial cell adhesion molecules E-selectin, VCAM-1 and ICAM-1 at sites of inflammation in vivo is due in whole or part to the upregulation of transcription of their respective genes. Pharmacologic antagonism of transcription from these genes may therefore represent a novel approach to the development of anti-inflammatory therapeutics. This paper reviews our current understanding of nuclear factors which act to regulate the transcriptional activity of the E-selectin, VCAM-1 and ICAM-1 genes, and discusses that evidence which suggests that the nuclear transcription factor NF-kappa B acts as a dominant regulator of transcription from these genes.
Chen
C C
CC
Cell Biology and Inflammation Research, Upjohn Laboratories, Kalamazoo, MI 49002, USA.
Manning
A M
AM
D001665:Binding Sites; D015815:Cell Adhesion Molecules / Q000235:genetics*; D004247:DNA / Q000378:metabolism; D019040:E-Selectin; D005786:Gene Expression Regulation; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D016328:NF-kappa B / Q000502:physiology*; D011401:Promoter Regions, Genetic; D014158:Transcription, Genetic; D019010:Vascular Cell Adhesion Molecule-1
D015815:Cell Adhesion Molecules; D019040:E-Selectin; D016328:NF-kappa B; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D004247:DNA