leukotriene-d4 has been researched along with Colitis* in 3 studies
3 other study(ies) available for leukotriene-d4 and Colitis
| Article | Year |
|---|---|
Structural Basis for Developing Multitarget Compounds Acting on Cysteinyl Leukotriene Receptor 1 and G-Protein-Coupled Bile Acid Receptor 1.
G-protein-coupled receptors (GPCRs) are the molecular target of 40% of marketed drugs and the most investigated structures to develop novel therapeutics. Different members of the GPCRs superfamily can modulate the same cellular process acting on diverse pathways, thus representing an attractive opportunity to achieve multitarget drugs with synergic pharmacological effects. Here, we present a series of compounds with dual activity toward cysteinyl leukotriene receptor 1 (CysLT Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Colitis; Humans; Leukotriene D4; Macrophages; Mice; Molecular Docking Simulation; Protein Binding; RAW 264.7 Cells; Receptors, G-Protein-Coupled; Receptors, Leukotriene; Structure-Activity Relationship | 2021 |
Identification of cysteinyl-leukotriene-receptor 1 antagonists as ligands for the bile acid receptor GPBAR1.
The cysteinyl leukotrienes (CysLTs), i.e. LTC Topics: Acetates; Animals; Anti-Inflammatory Agents, Non-Steroidal; Bile Acids and Salts; Colitis; Cyclopropanes; Disease Models, Animal; Gene Expression; Genes, Reporter; HEK293 Cells; Hep G2 Cells; Humans; Leukotriene Antagonists; Leukotriene C4; Leukotriene D4; Leukotriene E4; Luciferases; Mice; Mice, Knockout; Molecular Docking Simulation; Quinolines; RAW 264.7 Cells; Receptors, G-Protein-Coupled; Receptors, Leukotriene; Recombinant Fusion Proteins; Sulfides | 2020 |
Leukotriene D4-induced adhesion of Caco-2 cells is mediated by prostaglandin E2 and upregulation of alpha2beta1-integrin.
Cell-cell and extracellular matrix adhesions play important roles in the progression of cancer. We investigated the involvement of the inflammatory mediator leukotriene D4 (LTD4) in the regulation of cell-matrix adhesion of colon cancer (Caco-2) cells. We observed that LTD4 acted via its CysLT1 receptor in these cells to induce increased adhesion to collagen I. LTD4 also enhanced the activation and expression of alpha2beta1-integrins on the cell surface, which we found to be responsible for mediating the increased adhesion to collagen I. LTD4 simultaneously augmented expression of the prostaglandin-generating enzyme cyclooxygenase-2 (COX-2) and increased prostaglandin E2 (PGE2) production in Caco-2 cells. The adhesive capacity of the Caco-2 cells was reduced by specific inhibition of COX-2 and was subsequently restored by PGE2, but not by LTD4. A selective PGE2 receptor antagonist abolished the increased adhesion and the augmented alpha2beta1-integrin expression induced by both PGE2 and LTD4. Summarizing, the inflammatory mediator LTD4 regulates the adhesive properties and migration of the Caco-2 cell line by upregulating COX-2 and stimulating PGE2-induced expression of alpha2beta1-integrins. This suggests that inflammatory mediators such as LTD4 can be involved in the dissemination and survival of colon cancer cells. Topics: Caco-2 Cells; Carcinoma; Cell Adhesion; Colitis; Collagen Type I; Colonic Neoplasms; Cyclooxygenase 2; Dinoprostone; Extracellular Matrix; Humans; Integrin alpha2beta1; Isoenzymes; Leukotriene D4; Membrane Proteins; Nitrobenzenes; Prostaglandin-Endoperoxide Synthases; Receptors, Leukotriene; Sulfonamides; Up-Regulation; Xanthenes; Xanthones | 2003 |