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Leis, HJ; Windischhofer, W.
Ionomycin induces prostaglandin E2 formation in murine osteoblastic MC3T3-E1 cells via mechanisms independent of its ionophoric nature.
Biochem Cell Biol. 2016; 94(3):236-240
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Autor/innen der Med Uni Graz:
Leis Hans-Jörg
Windischhofer Werner
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Abstract:
Ionomycin and A23187 are divalent cation ionophores with a marked preference for calcium. Studies using these ionophores have almost exclusively interpreted their results in the light of calcium elevation. It was the aim of this study to investigate the effects of ionomycin in osteoblatic MC3T3-E1 cells that are not attributable to its ionophoric properties. Thus, we have found that in contrast to A23187, ionomycin shows similar effects on prostaglandin E2 formation as bradykinin and endothelin-1, being potentiated by extracellular nickel and inhibited by cholera toxin and pertussis toxin. Our data strongly suggest that inomycin, at least in part, exerts its effects via specific binding to a G-protein coupled receptor, thereby evoking downstream cellular events like arachidonate release with subsequent prostaglandin formation.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Bradykinin - pharmacology
Calcimycin - pharmacology
Calcium - pharmacology
Calcium Ionophores - pharmacology
Cell Line -
Cholera Toxin - pharmacology
Dinoprostone - biosynthesis
Dinoprostone - metabolism
Ionomycin - pharmacology
Mice -
Nickel - pharmacology
Osteoblasts - drug effects
Osteoblasts - metabolism
Pertussis Toxin - pharmacology
Receptors, G-Protein-Coupled - metabolism

Find related publications in this database (Keywords)
ionomycin
A23187
prostaglandin
nickel
osteoblast
MC3T3-E1
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