ArticleBritish journal of pharmacology2006
Substance P-induced cyclooxygenase-2 expression in human umbilical vein endothelial cells.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- Review
- Role of Sensory Nerves in Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Suppressing the Substance P-NK1R Signalling Protects Mice against Sepsis-Associated Acute Inflammatory Injury and Ferroptosis in the Liver and Lungs.Antioxidants (Basel, Switzerland) · 2024Article
- The In Vitro Pro-inflammatory Functions of the SP/NK1R System in Prostate Cancer: a Focus on Nuclear Factor-Kappa B (NF-κB) and Its Pro-inflammatory Target Genes.Applied biochemistry and biotechnology · 2023Article
- Can aprepitant used for nausea and vomiting be good gastrointestinal complaints?Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- Bergapten inhibits chemically induced nociceptive behavior and inflammation in mice by decreasing the expression of spinal PARP, iNOS, COX-2 and inflammatory cytokines.Inflammopharmacology · 2019Article
- The Neurokinin-1 Receptor Contributes to the Early Phase of Lipopolysaccharide-Induced FeverFrontiers in immunology · 2018Article
- Role of neurokinin type 1 receptor in nociception at the periphery and the spinal level in the rat.Spinal cord · 2016Article
- Ginsenoside Rg5:Rk1 attenuates TNF-α/IFN-γ-induced production of thymus- and activation-regulated chemokine (TARC/CCL17) and LPS-induced NO production via downregulation of NF-κB/p38 MAPK/STAT1 signaling in human keratinocytes and macrophages.In vitro cellular & developmental biology. Animal · 2016Article
- Ethanol Extract of Peanut Sprout Exhibits a Potent Anti-Inflammatory Activity in Both an Oxazolone-Induced Contact Dermatitis Mouse Model and Compound 48/80-Treated HaCaT Cells.Annals of dermatology · 2015Article
- Article
- Activation of satellite glial cells in rat trigeminal ganglion after upper molar extraction.Acta histochemica et cytochemica · 2009Article
- Common pathways for activation of proinflammatory gene expression by G protein-coupled receptors in primary lung epithelial and endothelial cells.Experimental lung research · 2009Article
- Tachykinin receptor modulation of cyclooxygenase-2 expression in human polymorphonuclear leucocytes.British journal of pharmacology · 2009Article
- Substance P upregulates LTB4 in rat adherent macrophages from granuloma induced by KMnO4.Neurotoxicity research · 2009Article
- An FDA approved neurokinin-1 receptor antagonist is effective in reducing intraabdominal adhesions when administered intraperitoneally, but not orally.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2008Article
- Substance P-mediated expression of the pro-angiogenic factor CCN1 modulates the course of colitis.The American journal of pathology · 2008Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Substance P (SP) is a neuropeptide involved in neurogenic inflammation and an agonist for NK(1), NK(2), and NK(3) receptors. SP induces prostaglandin (PG) production in various cell types, and these eicosanoids are responsible for numerous inflammatory and vascular effects. Cyclooxygenase (COX) are needed to convert arachidonic acid to PGs. The study evaluated the effect of SP on COX expression in human umbilical vein endothelial cells (HUVEC). COX-2 protein expression was upregulated by SP with a peak at 100 nM and at 20 h; in the same experimental conditions COX-1 protein expression was unchanged. A correlation between COX-2 expression and PGI(2) and PGE(2) release was detected. Dexamethasone (DEX) inhibited SP-mediated COX-2 expression. Mitogen-activated protein kinases (MAPK) p38 and p42/44 were activated by SP, whereas SB202190 and PD98059, inhibitors of these kinases, blocked COX-2 expression. 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulphonyl)phenyl-2(5H)-furanone (DFU), an experimental selective COX-2 inhibitor, blocked SP-induced PG release. By RT-PCR and Western blot analysis, we demonstrated that NK(1) and NK(2) but not NK(3) receptors are present on HUVEC. Selective NK(1) and NK(2) agonists, namely [Sar(9), Met(O(2))(11)]SP and [beta-Ala(8)] NKA(4-10), upregulated COX-2 protein expression and PG production, whereas senktide (Suc-Asp-Phe-MePhe-Gly-Leu-Met-NH(2)), a selective NK(3) agonist, was ineffective in this respect. The NK(1) selective antagonist L703,606 ((cis)-2-(diphenylmethyl)-N-((2-iodophenyl)-methyl)-1-azabicyclo(2.2.2)octan-3-amine) and the NK(2) selective antagonist SR 48,968 ((S)-N-methyl-N-(4-(4-acetylamino-4-phenylpiperidino)-2-(3,4 dichlorophenyl)butyl) benzamide) competitively antagonised SP-induced effects. The study shows HUVEC to possess functional NK(1) and NK(2) receptors, which mediate the ability of SP to induce expression of COX-2 in HUVEC, thus showing a previously-undetected effect of SP on endothelial cells.
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