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Details for phenotype: regulation of inflammatory response

EndoNet ID: ENP00300

Name

regulation of inflammatory response

General information

This phenotype is not pathologic

Links to other resources

GO
MeSH term 68007249

Phenotype triggers

  • more activity (high ligand concentration, overexpression) of Lysophosphatidic acid receptor 3
    in microglial_cell_in_central_nervous_system
    • It is notable that LPA3 is upregulated in lipopolysaccharide-stimulated microglia, suggesting a role for LPA signaling in activated microglia during neuroinflammation. [1]
  • normal activity of PRLR
    in prostate
    • The effects of PRL on prostate include involvement in estrogen-induced inflammation. [2]
    • Estradiol-induced inflammation in the rat lateral prostate is mediated at least in part by the release of PRL from the pituitary. [2]
  • normal activity of ER-alpha
    in macrophage
    • ER alpha is critical for maintenance of macrophage metabolism and for macrophage IL-4 responsiveness. [3]
    • ER alpha is necessary for the repression of inflammation, maintenance of oxidative metabolsim and full phagocytic activity in isolated macrophages. [3]
  • normal activity of ER-beta
    in microglial_cell_in_central_nervous_system
    • ER beta specific ligands potently inhibit transcriptional activation of inflammatory response genes in microglia and astrocytes. [4]
  • normal activity of Sphingosine 1-phosphate receptor 3
    in smooth_muscle_cell
    • In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression. [5]
  • normal activity of Sphingosine 1-phosphate receptor 1
    in smooth_muscle_cell
    • In vascular smooth muscle cells, S1P stimulates DNA synthesis in association with ERK activation, and may play a central role in excessive fibroproliferative and inflammatory response to vascular injury that are hallmarks of atherosclerois progression. [5]
    • a central role for S1P1 in vascular smooth muscle cell migration was established by the phenotype of S1P1-deficient mice in which those cells do not migrate properly to surround and reinforce nascent vessels. [6]
Reference