Inhibitor of protein tyrosine kinase, radicicol, suprresses the expression of cyclooxygenase and pro-inflammatory cytokines in LPS-stimulated rat alveolar macrophage in part by accelerating degradation of mRNA

L. Feng, B. C. Jang, D. Hwang

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

The protein tyrosine kinase inhibitor, radicicol, inhibits the expression of COX-2, TNFa, and IL-1b in LPS-stimulated rat alveolar macrophages. However, it did not inhibit the expression of the tyrosine phosphatase (3CH134) dephosphorylating MAP kinases. The inhibition of COX-2 expression by radicicol appears to occur to mainly at post-transcriptional steps. The inhibition of TNFa and IL-1b expression by radicicol is at least in part due to accelerated decay of mRNA. Radicicol also inhibits tyrosine phosphorylation of MAP kinases. However, whether the activation of MAP kinases is required for the expression of COX-2, TNFa, and IL-lb is not known. The proximal step in LPS-induced signaling pathways leading to the expression of COX-2, TNFa, IL-lb and perhaps other immediate early genes contains tyrosine kinase(s) that can be inhibited by radicicol. One of these upstream tyrosine kinases appears to be p53/56(lyn).

Original languageEnglish (US)
Pages (from-to)281-288
Number of pages8
JournalAdvances in Experimental Medicine and Biology
Volume407
StatePublished - 1996
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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