Neuropeptide Y promotes TGF-beta1 production in RAW264.7 cells by activating PI3K pathway via Y1 receptor.
- Author:
Jiang-Rui ZHOU
1
;
Zheng XU
;
Chun-Lei JIANG
Author Information
- Publication Type:Journal Article
- MeSH: Androstadienes; pharmacology; Animals; Blotting, Western; Cell Count; Cell Line; Cell Survival; drug effects; immunology; Enzyme Activation; drug effects; physiology; Enzyme-Linked Immunosorbent Assay; Immunosuppressive Agents; pharmacology; Macrophages; drug effects; immunology; metabolism; Mice; Neuropeptide Y; metabolism; pharmacology; Phosphatidylinositol 3-Kinases; drug effects; metabolism; Phosphorylation; drug effects; Receptors, Neuropeptide Y; agonists; metabolism; Signal Transduction; drug effects; immunology; Transforming Growth Factor beta1; agonists; metabolism; Up-Regulation; drug effects; immunology
- From: Neuroscience Bulletin 2008;24(3):155-159
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo examine the effect of neuropeptide Y (NPY) on TGF-beta1 production in RAW264.7 macrophages.
METHODSEnzyme linked immunosorbent assay (ELISA) was used to detect TGF-beta1 production. Cell counting kit 8 (CCK-8) was used to assay the viability of RAW264.7 cells. Western blot was used to detect the phosphorylation of PI3K p85.
RESULTSNPY treatment could promote TGF-beta1 production and rapid phosphorylation of PI3K p85 in RAW264.7 cells via Y1 receptor. The elevated TGF-beta1 production induced by NPY could be abolished by wortmannin pretreatment.
CONCLUSIONNPY may elicit TGF-beta1 production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.
