The oxygen radical scavenger pyrrolidine dithiocarbamate enhances interleukin-1beta-induced cyclooxygenase-2 expression in cerebral microvascular smooth muscle cells.
Oxidative stress and inducible cyclooxygenase-2 (COX-2)-mediated prostaglandin (PG) formation have been proposed to play an important role in cytokine-induced vascular pathology. To explore the relationship between oxidative stress and COX-2 induction, cultured murine cerebral microvascular smooth muscle cells (SMCs) were stimulated with interleukin-1beta (IL-1beta) in the presence or absence of an oxygen radical scavenger, pyrrolidine dithiocarbamate (PDTC). IL-1beta increased COX-2 protein expression in a dose- and time-dependent manner, an increase that was further enhanced by PDTC in a dose-dependent manner. PDTC did not, however, affect the expression of COX-1 protein. In the presence of 100 microM PDTC, PGE(2) production induced by IL-1beta (5 ng/ml) was increased by threefold as compared with IL-1beta alone. Although PDTC enhanced COX-2 protein expression, it did not increase IL-1beta- induced expression of COX-2 mRNA, indicating that the regulatory effect occurred at the posttranscriptional level. The time course of COX-2 protein degradation indicated that PDTC also did not alter the stability of the COX-2 protein induced by IL-1beta. These results suggest that endogenous oxygen radicals may blunt COX-2 induced by IL-1beta through an effect on translation.[1]References
- The oxygen radical scavenger pyrrolidine dithiocarbamate enhances interleukin-1beta-induced cyclooxygenase-2 expression in cerebral microvascular smooth muscle cells. Fang, X., Chen, P., Moore, S.A. Microvasc. Res. (2002) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
