ArticleThe Biochemical journal1995
Involvement of tyrosine kinases in the induction of cyclo-oxygenase-2 in human endothelial cells.
Article in The Biochemical journal, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 67 citations in OpenAlex.
- Soy food supplementation, dietary fat reduction and peripheral blood gene expression in postmenopausal women--a randomized, controlled trial.Molecular nutrition & food research · 2011Trial
- Inhibition of prostaglandin synthesis and actions by genistein in human prostate cancer cells and by soy isoflavones in prostate cancer patients.International journal of cancer · 2009Trial
- TNFα-activated stromal COX-2 signalling promotes proliferative and invasive potential of colon cancer epithelial cells.Cell proliferation · 2013Article
- Cancer prevention with promising natural products: mechanisms of action and molecular targets.Anti-cancer agents in medicinal chemistry · 2012Review
- Preconditioning mediated by sublethal oxygen-glucose deprivation-induced cyclooxygenase-2 expression via the signal transducers and activators of transcription 3 phosphorylation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2008Article
- Ischemic preconditioning via epsilon protein kinase C activation requires cyclooxygenase-2 activation in vitro.Neuroscience · 2007Article
- Discovery of a new function of cyclooxygenase (COX)-2: COX-2 is a cardioprotective protein that alleviates ischemia/reperfusion injury and mediates the late phase of preconditioning.Cardiovascular research · 2002Review
- Rethinking breast cancer risk and the environment: the case for the precautionary principle.Environmental health perspectives · 1998Article
- Roles for interleukin-1beta, phorbol ester and a post-transcriptional regulator in the control of bradykinin B1 receptor gene expression.The Biochemical journal · 1998Article
- Protein-tyrosine-kinase-dependent expression of cyclo-oxygenase-1 and -2 mRNAs in human endothelial cells.The Biochemical journal · 1997Article
- Review
- Cyclooxygenase-2 and its regulation in inflammation.Mediators of inflammation · 1996Article
- Cyclooxygenase-2 modulates cellular growth and promotes tumorigenesis.Journal of cellular and molecular medicineReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to a constitutive cyclo-oxygenase (Cox-1), human endothelial cells also possess an inducible cyclo-oxygenase (Cox-2) which plays an important role in the regulation of the synthesis of prostacyclin (prostaglandin I2). Cox-2 is regulated and expressed in large quantities upon activation of the cells by inducers such as phorbol myristate acetate (PMA), an activator of protein kinase C (PKC), or interleukin-1 alpha. We have investigated the involvement of protein tyrosine kinases in Cox-2 expression by human endothelial cells upon activation by these inducers. PMA or interleukin-1 alpha provoke an increase in the phosphorylation of substrates of 110 and 120 kDa and additional phosphorylations for a broad band of multiple substrates in the 70 kDa range. This stimulation was accompanied by the induction of Cox-2 protein, detectable after stimulation for 1 h, which is consistent with an increase in activity reflected by prostacyclin synthesis; no variation in the expression of Cox-1 could be observed. Three distinct inhibitors of protein tyrosine kinases, genistein, herbimycin or AG-213, reduced tyrosine phosphorylation of cell substrates, consistently with their pharmacological effects. Under these conditions, there was selective reduction of Cox-2 expression without modification of Cox-1. Regulation of Cox-2 induction is also dependent on the activation of PKC since Ro 31-8220 or PKC depletion by PMA prevented its induction. Our results suggest that within the time-frame of our experiments these effects on kinases are specific for Cox-2 rather than Cox-1.
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