Transduction of a signal for arachidonic acid metabolism by untriggered CSF-1 receptor induces an opposite effect to that induced by CSF-1 receptor and its ligand: Separate regulation of phospholipase A 2 and cyclooxygenase by CSF-1 receptor/CSF-1
Prostaglandins, Leukotrienes and Essential Fatty Acids, ISSN: 0952-3278, Vol: 45, Issue: 1, Page: 43-48
1992
- 3Citations
- 9Captures
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Article Description
The mouse hematopoietic cell line, 32D, was transfected with c-fms, which encodes for the CSF-1 receptor, a tyrosine kinase (TK). In the absence of CSF-1, transfected cells show moderate levels of arachidonic acid (AA) release and produce a substantial amount of prostaglandin E 2 (PGE 2 ) in comparison with the original cell line. Exposure of transfected cells to CSF-1, while inducing a substantial increase in arachidonate release, nevertheless resulted in inhibition of PGE 2 production. Addition of ST638, a tyrosine kinase inhibitor, to cells transfected with c-fms in the absence of CSF-1 inhibited PGE 2 production within 10–60 min. Its addition to the same cells in the presence of CSF-1 induced an opposite effect, but required longer treatment (24 h). In either cell type, AA release was not affected by this agent. These data indicate that CSF-1 may regulate cyclooxygenase activity. The different effect of CSF-1 receptor on PGE 2 production in the presence or absence of CSF-1 and the opposite effect of a tyrosine kinase inhibitor on PGE 2 suggest that both the receptor alone or the receptor-ligand complex may transduce an active, but different, signal through tyrosine phosphorylation. CSF-1 receptor and CSF-1 may exert separate, but related, effects on phospholipase A 2 and cyclooxygenase activity which, in concert, or along with other tyrosine kinases, regulate prostaglandin production.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/095232789290101N; http://dx.doi.org/10.1016/0952-3278(92)90101-n; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0026512752&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/1532099; http://linkinghub.elsevier.com/retrieve/pii/095232789290101N; http://api.elsevier.com/content/article/PII:095232789290101N?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:095232789290101N?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/095232789290101N; http://dx.doi.org/10.1016/0952-3278%2892%2990101-n; https://dx.doi.org/10.1016/0952-3278%2892%2990101-n
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