Transcriptional regulation of human CC chemokine CCL15 gene by NF-kappaB and AP-1 elements in PMA-stimulated U937 monocytoid cells

Biochim Biophys Acta. 2005 Dec 30;1732(1-3):38-42. doi: 10.1016/j.bbaexp.2005.11.001. Epub 2005 Dec 1.

Abstract

CCL15 exerts biological effects on a variety of cells, including monocytes. NF-kappaB has been reported to be involved in the transcription of the CCL15 gene. In this study, we have identified an AP-1 element located at -76/-65, which appears to regulate the transcription of the CCL15 gene. We also confirmed that the AP-1 factor binds to the element. Specific inhibitors for MAPK pathways and expression of dominant negative MKK4 or JNK1 reduced PMA-induced transcriptional activation of CCL15. Our findings indicate that transcription of the CCL15 gene is regulated by AP-1 and NF-kappaB through MEK and JNK MAPK pathways in monocytoid cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chemokines, CC / genetics*
  • Gene Expression Regulation / drug effects*
  • Humans
  • Macrophage Inflammatory Proteins
  • Monocytes / drug effects
  • Monocytes / metabolism*
  • Monokines / genetics*
  • NF-kappa B / metabolism*
  • Point Mutation / genetics
  • Promoter Regions, Genetic / drug effects
  • Protein Binding
  • Response Elements / genetics*
  • Signal Transduction / drug effects
  • Tetradecanoylphorbol Acetate / pharmacology
  • Transcription Factor AP-1 / metabolism*
  • Transcription, Genetic / drug effects*
  • U937 Cells

Substances

  • CCL15 protein, human
  • Chemokines, CC
  • Macrophage Inflammatory Proteins
  • Monokines
  • NF-kappa B
  • Transcription Factor AP-1
  • Tetradecanoylphorbol Acetate