Effect of glucagon like peptide-1 on proliferation and differentiation of endothelial progenitor cells and its mechanism.
10.3969/j.issn.1672-7347.2010.12.009
- Author:
Xiaoyun XIE
1
;
Zhaohui MO
;
Ke CHEN
;
Honghui HE
;
Yanhong XIE
Author Information
1. Department of Endocrinology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
- Publication Type:Journal Article
- MeSH:
Cell Differentiation;
drug effects;
Cell Proliferation;
drug effects;
Endothelial Cells;
cytology;
Glucagon-Like Peptide 1;
pharmacology;
Humans;
Leukocytes, Mononuclear;
cytology;
Stem Cells;
cytology;
metabolism;
Vascular Endothelial Growth Factor A;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2010;35(12):1254-1260
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect and mechanism of glucagon like peptide 1(GLP-1)on the proliferation and differentiation of endothelial progenitor cells(EPCs)derived from the peripheral blood.
METHODS:Mononuclear cells were isolated from human peripheral blood by density gradient centrifugation. After 7 days of culture,attached cells were stimulated with different cultures of 0.2% BSA,and GLP-1(1,10,and 20 nmol/L). Laser scanning confocal microscope was used to determine the EPCs from human peripheral blood.The activity of EPCs was observed under reverse microscope. MTT was used to determine the proliferation of EPCs. The expression of KDR,Flt-1,VE-cadherin,and eNOS mRNA was detected by RT-PCR.The concentration of serum VEGF was detected by ELISA. The expression of VEGF protein was detected by immunohistochemical SP method. The EPCs cultured in GLP-1 were intervened by VEGFmAb.
RESULTS:EPCs was proliferated more in the GLP-1 group(1,10,and 20 nmol/L) than in the control group (P<0.05 or P<0.01). The expression of KDR,FLT-1,VE-cadherin,eNOS mRNA and VEGF protein was higher than that in the control group(P<0.05 or P<0.01). VEGFmAb(100 ng/mL)down-regulated the expression of KDR,Flt-1,VE-cadherin,and eNOS mRNA.
CONCLUSION:GLP-1 can promote the proliferation and differentiation of EPCs derived from the peripheral blood by up-regulating VEGF autocrine.
