Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.

Isolated BALB/c mouse thioglycollate-elicited (inflammatory) peritoneal macrophages release at least 10 times more C1q than do isolated resident peritoneal macrophages. Addition of non-steroidal anti-inflammatory drugs (NSAID) to thioglycollate-elicited macrophages in culture inhibited the release o...

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Main Authors: Trinder, P K, Faust, D, Petry, F, Loos, M
Formato: Artigo
Idioma:English
Publicado em: 1995
Assuntos:
Research Article
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC1415162/
https://ncbi.nlm.nih.gov/pubmed/7790039
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spelling pubmed-14151622007-02-06 Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase. Trinder, P K Faust, D Petry, F Loos, M Immunology Research Article Isolated BALB/c mouse thioglycollate-elicited (inflammatory) peritoneal macrophages release at least 10 times more C1q than do isolated resident peritoneal macrophages. Addition of non-steroidal anti-inflammatory drugs (NSAID) to thioglycollate-elicited macrophages in culture inhibited the release of C1q and reduced levels of C1q-specific mRNA. Contrastingly, the NSAID were found to enhance C1q-specific mRNA levels in resident macrophages, although no increase in C1q levels secreted was observed. This suggests that the response of macrophages to NSAID, with respect to C1q synthesis, reflects the developmental stage of the macrophage. The gold salt auranofin (AFN) was found to enhance markedly C1q synthesis at both transcriptional and secretory levels in thioglycollate-elicited macrophages whilst, conversely, AFN reduced mRNA levels in resident macrophages. This indicates that AFN and the NSAID may work via the same or similar biochemical pathway, but with opposing effects. The glucocorticoid hydrocortisone (HC) greatly enhanced C1q-specific mRNA levels in both thioglycollate-elicited and resident macrophages, although no parallel increases in C1q secreted were observed. The data on inhibition of C1q biosynthesis by NSAID in thioglycollate-elicited macrophages are supported by the enhancement of C1q biosynthesis following addition of prostaglandin E2 (PGE2) or dibutyryl cyclic AMP (dBcAMP) to the cultures. From these experiments, it is concluded that C1q biosynthesis is controlled, at least in part, by a pathway involving cAMP. 1995-04 /pmc/articles/PMC1415162/ /pubmed/7790039 Text en
institution US National Library of Medicine
collection PubMed Central
language English
format Article
topic Research Article
spellingShingle Research Article
Trinder, P K
Faust, D
Petry, F
Loos, M
Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
description Isolated BALB/c mouse thioglycollate-elicited (inflammatory) peritoneal macrophages release at least 10 times more C1q than do isolated resident peritoneal macrophages. Addition of non-steroidal anti-inflammatory drugs (NSAID) to thioglycollate-elicited macrophages in culture inhibited the release of C1q and reduced levels of C1q-specific mRNA. Contrastingly, the NSAID were found to enhance C1q-specific mRNA levels in resident macrophages, although no increase in C1q levels secreted was observed. This suggests that the response of macrophages to NSAID, with respect to C1q synthesis, reflects the developmental stage of the macrophage. The gold salt auranofin (AFN) was found to enhance markedly C1q synthesis at both transcriptional and secretory levels in thioglycollate-elicited macrophages whilst, conversely, AFN reduced mRNA levels in resident macrophages. This indicates that AFN and the NSAID may work via the same or similar biochemical pathway, but with opposing effects. The glucocorticoid hydrocortisone (HC) greatly enhanced C1q-specific mRNA levels in both thioglycollate-elicited and resident macrophages, although no parallel increases in C1q secreted were observed. The data on inhibition of C1q biosynthesis by NSAID in thioglycollate-elicited macrophages are supported by the enhancement of C1q biosynthesis following addition of prostaglandin E2 (PGE2) or dibutyryl cyclic AMP (dBcAMP) to the cultures. From these experiments, it is concluded that C1q biosynthesis is controlled, at least in part, by a pathway involving cAMP.
author Trinder, P K
Faust, D
Petry, F
Loos, M
author_facet Trinder, P K
Faust, D
Petry, F
Loos, M
author_sort Trinder, P K
title Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
title_short Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
title_full Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
title_fullStr Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
title_full_unstemmed Modulation of mRNA expression and secretion of C1q in mouse macrophages by anti-inflammatory drugs and cAMP: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin E2 and adenylate cyclase.
title_sort modulation of mrna expression and secretion of c1q in mouse macrophages by anti-inflammatory drugs and camp: evidence for the partial involvement of a pathway that includes cyclooxygenase, prostaglandin e2 and adenylate cyclase.
publishDate 1995
url https://ncbi.nlm.nih.gov/pmc/articles/PMC1415162/
https://ncbi.nlm.nih.gov/pubmed/7790039
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