Tumor necrosis factor-alpha regulates the proliferation and syndecan-4 expression of human umbilical vein endothelial-like cells cultured in vitro.
- Author:
Bin ZHANG
1
;
Ping OUYANG
;
Ye CHEN
;
Wen-yan LAI
;
Jin-guo XIE
;
Ding-li XU
Author Information
- Publication Type:Journal Article
- MeSH: Cell Proliferation; Cells, Cultured; Endothelial Cells; metabolism; Humans; Syndecan-4; metabolism; Tumor Necrosis Factor-alpha; pharmacology; Umbilical Veins; cytology
- From: Journal of Southern Medical University 2007;27(4):496-498
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of tumor necrosis factor-alpha(TNF-alpha) on syndecan-4 protein expression and proliferation of cultured human umbilical vein endothelial-like cells (HUVECs) in vitro.
METHODSHUVECs exposed to different concentrations of TNF-alpha(100, 20, 10, and 1 ng/ml) were cultured for 24 h and 36 h to observe their proliferation in comparison with the control group. The cell proliferation rate was determined by non-radioactive MTS/PES assay. The expression of syndecan-4 protein was evaluated by immunoblotting technique using anti-syndecan-4 antibody. Results The proliferation rate of the endothelial-like cells was 1.956-/+0.214 in the control group, and 2.154-/+0.250, 2.260-/+0.151, 2.118-/+0.205 and 2.106-/+0.136 in TNF-alpha-treated groups corresponding to TNF-alpha concentrations of 100, 20, 10 and 1 ng/ml at 24 h, respectively. It was shown that TNF-alpha significantly stimulated cell proliferation at the concentration above 1 ng/ml (P<0.05) as compared with the control group (P<0.05). The proliferation rate of the endothelial-like cell was 1.915-/+0.236 in the control group, and 2.067-/+0.328, 2.207-/+0.150, 2.052-/+0.126 and 2.051-/+0.180 in TNF-alpha-treated groups corresponding to TNF-alphaconcentrations of 100, 20, 10 and 1 ng/ml at 36 h, respectively. The expression of syndecan-4 protein was significantly enhanced by TNF-alpha.
CONCLUSIONSTNF-alpha can stimulate HUVEC proliferation, and expression of syndean-4 may represent an additional component of the pro-inflammatory, growth-stimulating pathways that are activated in response to changes in the vascular wall.