Effect of C-reactive protein on Notch pathway components in human periphery blood endothelial progenitor cells.
- Author:
Aihua CHEN
1
;
Fei HE
;
Jing CHENG
;
Fulin LIU
;
Xudong SONG
;
Jingbin GUO
Author Information
- Publication Type:Journal Article
- MeSH: C-Reactive Protein; pharmacology; Calcium-Binding Proteins; genetics; metabolism; Cell Adhesion; Cell Movement; Cell Proliferation; Cells, Cultured; Endothelial Cells; cytology; metabolism; Humans; Intercellular Signaling Peptides and Proteins; genetics; metabolism; Jagged-1 Protein; Leukocytes, Mononuclear; cytology; metabolism; Membrane Proteins; genetics; metabolism; RNA, Messenger; genetics; metabolism; Receptor, Notch1; genetics; metabolism; Serrate-Jagged Proteins; Signal Transduction; drug effects; Stem Cells; cytology; metabolism
- From: Journal of Southern Medical University 2012;32(2):239-242
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of C-reactive protein (CRP) on the expressions of Notch pathway components in human peripheral blood endothelial progenitor cells (EPC) in vitro.
METHODSMononuclear cells isolated by density gradient centrifugation of human peripheral blood mixed with 6% hydroxyethyl starch (Hes) were plated on fibronectin-coated 6-well culture dishes. After 7 days, the adherent cells were cultured in the presence of 10 and 20 mg/L CRP for 48 h, and the proliferation, migration, and adhesion abilities of the cells were observed. The mRNA expressions of Notch-1 and its ligand Jagged-1 in the EPCs were measured by RT-PCR, and their protein expressions by Western blotting.
RESULTSCRP at 10 and 20 mg/L caused a significant reduction in the number of viable EPCs (61∓3 and 54∓3, respectively) as compared with PBS (71∓4, P<0.05). CRP also resulted in a significant suppression of the proliferation, migration and adhesion capacities of the EPCs. The mRNA and protein expressions of Jagged-1 and Notch-1 in the EPCs significantly increased following CRP exposure in comparison with PBS treatment.
CONCLUSIONCRP can suppress the proliferation, migration and adhesion capacities of the EPCs probably by affecting the expressions of the Notch-1 pathway components.
