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Cay10580

Manufactured by Cayman Chemical
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Sourced in United States

CAY10580 is a chemical compound that functions as a selective inhibitor of the enzyme cGMP-dependent protein kinase G (PKG). It is intended for use in research applications.

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Lab products found in correlation

Sulprostone, by Cayman Chemical (3 mentions) Butaprost, by Cayman Chemical (3 mentions) Nf κb inhibitor bay 11, by Merck Group (1 mentions) Ah23848, by Cayman Chemical (1 mentions) Ah6809, by Cayman Chemical (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Rolipram, by Merck Group (1 mentions) Celecoxib, by Merck Group (1 mentions) Efluor 670, by Thermo Fisher Scientific (1 mentions) Anti cd3 anti cd28 dynabeads, by Thermo Fisher Scientific (1 mentions) Lipopolysaccharide lps, by Merck Group (1 mentions) Matrigel, by Corning (1 mentions) Sulprostone, by Merck Group (1 mentions) Ono 8711, by Cayman Chemical (1 mentions) Transwell, by Corning (1 mentions) Gw627368, by Cayman Chemical (1 mentions) Sc 51089, by Cayman Chemical (1 mentions) L 161 982, by Cayman Chemical (1 mentions) Indomethacin, by Merck Group (1 mentions) Trypsin, by Thermo Fisher Scientific (1 mentions)

4 protocols using cay10580

1

Evaluating PGE2 Receptor Agonists and Antagonists

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PGE2, purchased from Sigma (St. Louis, MO, USA) was dissolved in dimethyl sulfoxide (Sigma) and then diluted with complete medium to concentrations suitable for use in this experiment. The receptor agonists and antagonists, obtained from Cayman Chemical (Ann Arbor, MI) were as follows: EP1 receptor and EP3 receptor agonist (Sulprostone, 10 nM), EP2-receptor agonist (Butaprost, 10 µM), EP4 receptor agonist (CAY10580, 10 µM), EP2 receptor antagonist (AH6809, 10 µM) and the EP4 receptor antagonist (AH23848, 10 µM). Akt inhibitor (LY294002, 10 µM) was purchased from Calbiochem (Billerica, MA, USA). NF-κB inhibitor (BAY-11, 1 µM) was bought from Sigma. NPDFs were previously exposed to PGE2 (20 µM) after pre-treatment for 1 hour with all agonists, antagonists and inhibitors.
Cho J.S., Han I.H., Lee H.R, & Lee H.M. (2014). Prostaglandin E2 Induces IL-6 and IL-8 Production by the EP Receptors/Akt/NF-κB Pathways in Nasal Polyp-Derived Fibroblasts. Allergy, Asthma & Immunology Research, 6(5), 449-457.
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2

Inhibition of mPGES-1 in Immune Regulation

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The mPGES-1 inhibitor compound III (C3) (5 μM) [11 (link)] was synthesized by NovaSAID AB (Solna, Sweden). Celecoxib (5 μM), lipopolysaccharide (LPS) (50 ng/ml), dimethylsulfoxide (DMSO), and rolipram (10 μM) were purchased from Sigma-Aldrich (St.Louis, MO, USA). CD80 (5 μg/ml) and CD86 (5 μg/ml) neutralizing antibodies and the isotype control (5 μg/ml) were purchased from eBiosciences (Frankfurt, Germany) or R&D Systems (Minneapolis, MN, USA). PGE2, butaprost (5 μM), sulprostone (5 μM) and cay10580 (200 nM) were from Cayman Chemicals (Ann Arbor, MI, USA). Both human and murine interferon-γ (IFN-γ) (100 U/ml) were from Peprotech (Hamburg, Germany). Anti-CD3/anti-CD28 Dynabeads (1:20 - bead: PBMCs) were from Invitrogen (Carlsbad, Germany). OVA (257-267) SIINFEKEL was from Anaspec (Seraing, Belgium). Cell proliferation dye eFluor670 was from eBiosciences. Matrigel was from Corning Life Sciences (Amsterdam, Netherlands).
Olesch C., Sha W., Angioni C., Sha L.K., Açaf E., Patrignani P., Jakobsson P.J., Radeke H.H., Grösch S., Geisslinger G., von Knethen A., Weigert A, & Brüne B. (2015). MPGES-1-derived PGE2 suppresses CD80 expression on tumor-associated phagocytes to inhibit anti-tumor immune responses in breast cancer. Oncotarget, 6(12), 10284-10296.
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3

Induction of AQP2 expression in mpkCCD cells

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Mouse mpkCCDc14 cells were maintained essentially as described (Hasler et al., 2002 (link)). Cells were seeded at a density of 1.5 × 105 cells/cm2 on semipermeable filters (Transwell®, 0.4 μm pore size, Corning Costar, Cambridge, MA) and cultured for 8 days. Unless stated otherwise, the cells were exposed to 1 nM of the V2R agonist desmopressin (dDAVP) at the basolateral side during the last 96 h, to maximally induce the AQP2 expression (Li et al., 2006 (link)). Cells were incubated with 10 μM indomethacin, 1 μM PGE2 (both Sigma, St. Louis, MO, USA), 1 μM PGF2α (Calbiochem, San Diego, CA), 300 nM of EP1/EP3 agonists sulprostone (Sigma, St. Louis, MO, USA), 1 μM of EP4 agonists CAY10580, 0.5 μM of EP4 antagonist Gw627368, 2.5 nM of the EP4 antagonist L161982, 20 μM of EP1 antagonist Sc-51089, or 100 nM of EP1 antagonist Ono-8711 (all Cayman Chemical, Ann Arbor, Michigan, USA) during the last 48 h. The medium was replaced after 24 h, or in experiments using the EP agonists or antagonists, the medium was replaced every 12 h.
Deen P.M., Boone M., Schweer H., Olesen E.T., Carmone C., Wetzels J.F., Fenton R.A, & Kortenoeven M.L. (2022). A Vasopressin-Induced Change in Prostaglandin Receptor Subtype Expression Explains the Differential Effect of PGE2 on AQP2 Expression. Frontiers in Physiology, 12, 787598.
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4

Murine Mast Cell Signaling Pathway

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Murine MCs were kindly provided by donors Fudan University; cAMP and PGE2 ELISA kits were obtained from R&D; TGF-β1 was obtained from Peprotech; 17-phenyl PGE2 (EP1A, EP1 agonist, prostanoid receptor agonist selectivity: EP1>EP3), butaprost (EP2A, EP2 agonist), sulprostone (EP3A, prostanoid receptor agonist selectivity: EP3>EP1) and cay10580 (EP4A, EP4 agonist) were obtained from Cayman; Rabbit anti-phospho-p38 MAPK (Thr-180/Tyr-182), phospho-ERK1/2 (Thr-202/Tyr-204), phospho-JNK1/2 (T183/Y185), total JNK, total ERK1/2, total p38, p27kip1, cyclin D1, COX-2 were obtained from Cell Signaling Technology. Mouse anti-CCN2/connective tissue growth factor (CTGF), membrane-bound PGE synthase 1 (mPGES1), laminin (LN) were obtained from Abcam; Dulbecco's modified Eagle's medium, phosphate-buffered saline, trypsin, non-essential amino acids and antibiotics (penicillin/streptomycin) were obtained from Invitrogen; all solutions and instruments for RT-PCR were obtained from Applied Biosystems; 100-mm and 6-well cell culture plates were obtained from Fisher. The experimental protocol was approved by the Experimentation Ethics Committee of the Nantong University for the use of human or animal subjects.
Xi P.P., Xu Y.Y., Chen X.L., Fan Y.P, & Wu J.H. (2016). Role of the prostaglandin E2 receptor agonists in TGF-β1-induced mesangial cell damage. Bioscience Reports, 36(5), e00383.
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