Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1999-5-24
pubmed:abstractText
The ability of natural and synthetic opioids to modulate the induction of ornithine decarboxylase (ODC) was investigated in immune cells and cardiomyocytes in culture. In particular, Leu-enkephalin, which shows preference for delta-receptors, enhanced ODC activity in both thymocytes and cardiomyocytes, whereas the effect of U-50488H, a synthetic kappa-selective agonist, was cell-specific. In thymocytes, U-50488H markedly inhibited the induction of the enzyme elicited by the mitogen concanavalin A (Con A) or by a combined treatment with PMA and A23187, and also reduced basal ODC activity. However the drug did not affect ODC induced by other stimuli. The inhibition of the induction of ODC activity was accompanied by a reduction of ODC mRNA level and an acceleration of ODC turnover. The action of U-50488H in thymocytes does not appear to be mediated by kappa or other classical opioid receptors lacking both stereospecificity and antagonist sensitivity, but may involve a pertussis toxin-sensitive G protein. Splenocytes also showed the ODC inhibiting effect of U-50488H, although they were less sensitive compared to thymocytes. In contrast, U-50488H enhanced ODC activity in cardiomyocytes and this effect was blocked by a specific kappa-antagonist. In conclusion, these results indicate that some opioid agonists can modulate ODC expression in non neural cells. In particular, kappa-opioid receptors may be involved in the U-50488H action in cardiomyocytes, and a distinct site, linked to inhibition of cell proliferation, may operate in immune cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0300-8177
pubmed:author
pubmed:issnType
Print
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
47-53
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9746211-3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benz..., pubmed-meshheading:9746211-Analgesics, Non-Narcotic, pubmed-meshheading:9746211-Animals, pubmed-meshheading:9746211-B-Lymphocytes, pubmed-meshheading:9746211-Cells, Cultured, pubmed-meshheading:9746211-Enkephalin, Leucine, pubmed-meshheading:9746211-Enzyme Induction, pubmed-meshheading:9746211-Immune System, pubmed-meshheading:9746211-Ligands, pubmed-meshheading:9746211-Male, pubmed-meshheading:9746211-Myocardium, pubmed-meshheading:9746211-Organ Specificity, pubmed-meshheading:9746211-Ornithine Decarboxylase, pubmed-meshheading:9746211-RNA, Messenger, pubmed-meshheading:9746211-Rats, pubmed-meshheading:9746211-Rats, Wistar, pubmed-meshheading:9746211-Receptors, Opioid, pubmed-meshheading:9746211-T-Lymphocytes
pubmed:year
1998
pubmed:articleTitle
Modulation of the induction of ornithine decarboxylase by some opioid receptor agonists in immune cells and cardiomyocytes.
pubmed:affiliation
Dipartimento di Biochimica G. Moruzzi, Università di Bologna, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't