ep4 receptor antagonist 1  (MedChemExpress)

Journal: Journal of Lipid Research

Article Title: EBV promotes alveolar trabecula resorption via extracellular vesicle remodeling by group IIA secreted phospholipase A 2

doi: 10.1016/j.jlr.2026.101014

Figure Lengend Snippet: sPLA 2 -IIA hydrolyzes EV phospholipids and promotes bone resorption through LPAR1 and EP4 receptor. A: Electrospray ionization mass spectrometry of lipids from Akata LCL EVs after treatment with sPLA 2 -IIA (n = 3). Whole lipids were extracted, and the levels of both lysophospholipids and polyunsaturated fatty acids were analyzed. Relative values are shown. Values are presented as the mean ± SEM. Statistical significance was determined using student’s t test: ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001. B: THP-1 cells were cultured with Akata LCL EVs treated with or without sPLA 2 -IIA for 24 h. Prior to administration, THP-1 cells were pretreated with or without 10 μM AM966 or 1 μM EP4 receptor antagonist 1. C: Representative images of H&E staining, immunostaining of CTSK, and TRAP staining of the mouse maxillary palatal region. PBS, sPLA 2 -IIA, Akata LCL EVs, and sPLA 2 -IIA-treated Akata LCL EVs were injected into the mandibular incisor region. EVs are treated with sPLA 2 -IIA and varespladib prior to injection. Capitals indicate T: tooth, P: periodontal ligament, and B: bone region. A representative example is shown from the analysis of three mice. D: Quantification of CTSK and TRAP staining in the tissue shown in C (n = 3 mice per group). Values in B and D are presented as the mean ± SD. Statistical significance was determined using student’s t test: ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001.

Article Snippet: Akata LCL-derived EVs were added at a concentration corresponding to 5 μg of total protein per well and incubated at 37°C in a humidified atmosphere containing 5% CO 2 for 24 or 48 h. For inhibitor treatment, cells were pretreated with 10 μM AM966 (HY-15277, MedChemExpress) or 1 μM EP4 receptor antagonist 1 (HY-133123, MedChemExpress) 30 min prior to EV exposure.

Techniques: Mass Spectrometry, Cell Culture, Staining, Immunostaining, Injection

Journal: Stem cells (Dayton, Ohio)

Article Title: Human Mesenchymal Stem Cell-Derived Microvesicles Prevent the Rupture of Intracranial Aneurysm in Part by Suppression of Mast Cell Activation via a PGE2-Dependent Mechanism

doi: 10.1002/stem.2448

Figure Lengend Snippet: The anti-inflammatory role of EP4 in mediating the immunosuppressive effect of MVs. (A) MVs treatment altered the mRNA expression of EP 1-4 receptors in activated BMMCs (stimulated with A23187 (indicated as “Ca +”). EP1 and EP3 mediate the pro-inflammatory effects of PGE2 on mast cells but EP4 mediates anti-inflammatory responses. N = 6. (B, C) The administration of a selective EP4 receptor antagonist (GW 627368X, indicated as “GWX”) eliminated the suppressive effects of MVs on TNFα release in activated BMMCs (B) as well as the protective effects of MVs against rupture of intracranial aneurysms in mice (C) (N = 8 in each group). #p < 0.05 by t-test analysis; **p is significant by ANOVA with Bonferroni correction; *p < 0.05 by Fisher exact test.

Article Snippet: To study the role of PGE2 and EP receptors in the effect of MVs on mast cells, we utilized inhibitors, receptor antagonist, or exogenous PGE2 at different concentrations in vitro : NS-398 at 1, 10 μmol/L (Cyclooxygenase-2 (COX2) inhibitor, Cayman Chemicals), GW 627368X at 0.1, 1, 10 μmol/L (selective EP4 receptor antagonists, Cayman Chemicals) and PGE2 at 0.1, 1 μmol/L (Sigma-Aldrich).

Techniques: Expressing