Media of rat macrophage NR8383 cells with prostaglandins E2-induced VEGF over-expression promotes migration and tube formation of human umbilical vein endothelial cells.
- Author:
Mian LIU
1
;
Yi GONG
;
Jin-Yan WEI
;
Duo XIE
;
Jing WANG
;
Yan-Hong YU
;
Song QUAN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Line; Cell Movement; Cells, Cultured; Culture Media, Conditioned; pharmacology; Dinoprostone; pharmacology; Human Umbilical Vein Endothelial Cells; cytology; drug effects; Humans; Macrophages; chemistry; Neovascularization, Pathologic; RNA, Messenger; Rats; Receptors, Prostaglandin E, EP2 Subtype; metabolism; Receptors, Prostaglandin E, EP4 Subtype; metabolism; Vascular Endothelial Growth Factor A; Xanthones; pharmacology
- From: Journal of Southern Medical University 2016;36(7):936-940
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of prostaglandins E2 (PGE2) in enhancing vascular endothelial growth factor (VEGF) expression in a rat macrophage cell line and the effect of the media from PGE2-inuced rat macrophages on angiogenetic ability of human umbilical vein endothelial cells (HUVECs) in vitro.
METHODSWestern blotting and qPCR were employed to investigate the expressions of VEGF protein and mRNAs in rat macrophage cell line NR8383 stimulated by PGE2 in the presence or absence of EP2 receptor inhibitor (AH6809) and EP4 receptor inhibitor (AH23848). Conditioned supernatants were obtained from different NR8383 subsets to stimulate HUVECs, and the tube formation ability and migration of the HUVECs were assessed with Transwell assay.
RESULTSPGE2 stimulation significantly enhanced the expression of VEGF protein and mRNAs in NR8383 cells in a dose-dependent manner. The supernatants from NR8383 cells stimulated by PGE2 significantly enhanced tube formation ability of HUVECs (P<0.05) and promoted the cell migration. Such effects of PGE2 were blocked by the application of AH6809 and AH23848.
CONCLUSIONPGE2 can dose-dependently increase VEGF expression in NR8383 cells, and the supernatants derived from PGE2-stimulated NR8383 cells can induce HUVEC migration and accelerate the growth of tube like structures. PGE2 are essential to corpus luteum formation by stimulating macrophages to induce angiogenesis through EP2/EP4.
