ArticleBritish journal of pharmacology2009
Prostaglandin E2 induces contraction of liver myofibroblasts by activating EP3 and FP prostanoid receptors.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 12 citations in OpenAlex.
- Induction of myosin light chain kinase and CPI-17 by TGF-β accelerates contractile activity in intestinal epithelial cells.The Journal of veterinary medical science · 2018Article
- Protein kinase Cδ mediates histamine-evoked itch and responses in pruriceptors.Molecular pain · 2015Article
- Diverse effects of prostaglandin E₂ on vascular contractility.Heart and vessels · 2014Article
- Multifaceted roles of PGE2 in inflammation and cancer.Seminars in immunopathology · 2013Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeIncreased portal pressure in liver injury results from hypercontraction of perivascular non-parenchymal cells including liver myofibroblasts (MFs). Prostaglandin E2 (PGE2) is the major eicosanoid which is released around the venous system during liver injury, but little is known about their contractile effect on MFs. EXPERIMENTAL APPROACH: Contraction of primary rat liver MFs was measured by a collagen gel contraction assay. Expression of E prostanoid (EP) receptor subtypes was assessed by reverse transcription-polymerase chain reaction. Fura-2 fluorescence was used to determine intracellular Ca2+ concentration ([Ca2+](i)). Phosphorylation of protein kinase C (PKC) was detected by Western blot analysis. KEY
resultsLiver MFs expressed mRNAs for all four EP receptors. PGE2 induced contraction in a dose- and time-dependent manner, and slightly increased [Ca2+](i) only at high concentrations (10 micromol.L(-1)). An agonist selective for EP(3) receptors, ONO-AE-248, dose-dependently induced MF contraction but did not increase [Ca2+](i). Pretreatment with rottlerin (a specific novel PKC inhibitor) and Ro 31-8425 (a general PKC inhibitor) significantly reduced 1 micromol.L(-1) PGE(2)- or ONO-AE-248-induced contractions. Furthermore, 1 micromol.L(-1) PGE(2) stimulated phosphorylation of PKC isoforms PKCdelta and PKCepsilon. The F prostanoid (FP) receptor antagonist AL8810 abolished the [Ca(2+)](i) elevation and the rapid contraction induced by 10 micromol.L(-1) PGE2. CONCLUSIONS AND IMPLICATIONS: Lower concentrations up to 1 micromol.L(-1) of PGE2 induce liver MF contraction via a [Ca2+](i)-independent PKC-mediated pathway through the EP(3) receptor, while higher concentrations have an additional pathway leading to Ca(2+)-dependent contraction through activating the FP receptor.
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