Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add filters








Language
Year range
1.
The Korean Journal of Physiology and Pharmacology ; : 171-176, 2008.
Article in English | WPRIM | ID: wpr-728391

ABSTRACT

Heat shock proteins (HSPs) serve as molecular chaperones and play a role in cell protection from damage in response to stress stimuli. The aim of this article is to investigate whether HSP22 affects IL-8 expression in vascular smooth muscle cells (VSMCs), and which cellular factors are involved in the HSP-mediated IL-8 induction in that cell type in terms of mitogen activated protein kinase (MAPK) and transcription element. Exposure of aortic smooth muscle cells (AoSMCs) to HSP22 not only enhanced IL-8 release but also induced IL-8 transcript via promoter activation. HSP22 activated ERK and p38 MAPK in AoSMCs. HSP22-induced IL-8 release was inhibited by U0126, but not by SB202190. A mutation in the IL-8 promoter region at the binding site of NF-kappa B, but not AP-1 or C/EBP, impaired promoter activation in response to HSP22. Delivery of I kappa B, but not dominant negative c-Jun, lowered HSP22-induced IL-8 release from AoSMCs. These results suggest that HSP22 induces IL-8 in VSMCs via ERK1/2, and that transcription factor NF-kB may be required for the HSP22-induced IL-8 up-regulation.


Subject(s)
Binding Sites , Butadienes , Cytoprotection , Heat-Shock Proteins , Hot Temperature , I-kappa B Proteins , Imidazoles , Interleukin-8 , Molecular Chaperones , Muscle, Smooth, Vascular , Myocytes, Smooth Muscle , NF-kappa B , Nitriles , p38 Mitogen-Activated Protein Kinases , Promoter Regions, Genetic , Protein Kinases , Proteins , Pyridines , Shock , Transcription Factor AP-1
SELECTION OF CITATIONS
SEARCH DETAIL