Citation Details
Supression of endothelial adhesion molecule up-regulation with cyclopentenone prostaglandins is dissociated from IkappaB kinase inhibition and cell death induction
| Authors | Zernecke A, Erl W, Fraemohs L, Lietz M, Weber C |
| In | FASEB J (2003) 17(9): 1099-1101 |
| Substrate | Plasmid (general) |
| Reporter Gene | eGFP |
Nucleofection Experiments
During inflammation processes, like after TNF-alpha stimulation, various adhesive interactions between endothelial cells and the blood constituents are changed in order to recruit circulating leukocytes to the site of inflammation. The adhesive properties is mediated by cell surface proteins termed ?cell adhesion molecules? (CAM). The TNF-alpha-induced increased of CAM expression is regulated by NF-kappaB. In this regard cPG (cyclopentone prostaglandins) inhibit IkappaB-alpha kinase (IKK) which in turn inhibits apoptosis through NF-kappaB. To further elucidate this mechanisms the authors nucleofected HUVEC with an IKK mutant resistant to cPG. Cells were then treated with PGA1 (a cPG) and stimulated with TNF-alpha. CAM expression was analyzed by flow cytometry. The results indicate that IKK inhibition is not required for the suppression of endothelial CAM induction.
