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Cited by 178Inflammatory mediators and NSAID effectsEicosanoids and Hypertension PharmacologySignaling Pathways in Disease

The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index.

Interleukin-1-induced cyclooxygenase 2 expression is suppressed by cyclosporin A in rat mesangial cells

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Martin, Michael, Neumann, Detlef, Hoff, Torsten, Resch, Klaus, DeWitt, David L., Goppelt-Struebe, Margarete·1994·Kidney International
DOI 10.1038/ki.1994.18
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Abstract

The immunosuppressive drug cyclosporin A (CsA) has considerable nephrotoxic side effects which seem to be related to its interference with the synthesis of vasoactive prostanoids. Therefore, the molecular mechanism of the effect of CsA on the synthesis of prostaglandin E2 (PGE2) was investigated in rat renal mesangial cells (RMC). CsA effectively inhibited the PGE2 synthesis induced by inflammatory cytokines such as interleukin 1 (IL-1) or tumor necrosis alpha (TNF alpha). The induction by IL-1 and the inhibition by CsA were reflected in the enzyme activity of the cyclooxygenase. The changes in activity could be correlated with the expression of the inducible cyclooxygenase isoform (COX2), which is characterized by its 4.4 kb mRNA: the expression of this enzyme was enhanced by IL-1 and suppressed by CsA on the mRNA and protein level as determined by Northern and Western blot analyses. Suppression of COX2 mRNA was also observed when the message was induced by LPS or ionophore A23187. The expression of the basal cyclooxygenase isoform (COX1), which was constitutively expressed in proliferating mesangial cells, was not affected by IL-1 or CsA. Interferon gamma, which did not induce prostaglandin synthesis or influence COX mRNA expression, augmented the expression of MHC antigens in RMC. This induction was insensitive to CsA treatment. We could thus show that the inducible cyclooxygenase isoform in mesangial cells is a molecular target for CsA providing a possible mechanism for t…

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Metadata

Authors
Martin, M., Neumann, D., Hoff, T., Resch, K., DeWitt, D. L., & Goppelt-Struebe, M.
Affiliations
  • Medizinische Hochschule Hannover (DE)
  • Friedrich-Alexander-Universität Erlangen-Nürnberg (DE)
Corresponding author
Martin, Michael
ORCID
Neumann, Detlef
Venue
Kidney International
Publisher
Elsevier BV
Published
1994-01
Volume
45
Issue
1
Pages
150-158
ISSN
0085-2538 (ISSN-L)
DOI
10.1038/ki.1994.18
OpenAlex
W1965476867
Cited by
178
References
42
Citations by year
2025: 1 · 2023: 1 · 2022: 4 · 2020: 1 · 2015: 3 · 2014: 3 · 2013: 3 · 2012: 1
FWCI
10.44
Type
journal article
Language
en
Open access
Licence
Locations
  • Kidney International (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords
cyclosporine, cyclooxygenase-2, interleukin-1, renal mesangial cells, prostaglandin E2 synthesis, cyclooxygenase-1, TNF-α, interferon-gamma, MHC antigen expression, cyclosporine nephrotoxicity, inflammatory cytokines
MeSH terms
Animals, Histocompatibility Antigens Class II, Cells, Cultured, Glomerular Mesangium, Interleukin-1, Male, Prostaglandin-Endoperoxide Synthases, Recombinant Proteins, RNA, Messenger, Dinoprostone, Histocompatibility Antigens Class I, Cytokines, Cyclosporine, Cyclooxygenase Inhibitors, Rats, Sprague-Dawley, Rats

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