Cytokine Induced Differential Expression of Adhesion Molecules and HLA-DR in Cultured Human Glomerular Endothelial Cells.
- Author:
Su Kil PARK
1
;
Won Seok YANG
;
Hanjong AHN
;
Choung Soo KIM
;
Jong Soo LEE
;
Jae Dam LEE
Author Information
1. Department of Internal Medicine, College of Medicine, University of Ulsan, Seoul, Korea. skpark@www.amc.seoul.kr
- Publication Type:Original Article
- Keywords:
ICAM-1;
VCAM-1;
HLA-DR;
Glomerular endothelial cells;
IL-1 beta;
TNF-alpha;
IFN-gamma
- MeSH:
Carcinoma, Renal Cell;
Cytokines;
Endothelial Cells*;
Enzyme-Linked Immunosorbent Assay;
Factor VIII;
HLA Antigens;
HLA-DR Antigens*;
Humans*;
Intercellular Adhesion Molecule-1;
Interleukin-1beta;
Kidney;
Tumor Necrosis Factor-alpha;
Vascular Cell Adhesion Molecule-1
- From:Korean Journal of Nephrology
2001;20(2):221-228
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Glomerular endothelial cells should participate in the process of glomerular disease by expressions of HLA antigens and adhesion molecules. However, few have been known about the regulation of the expression of these molecules in human glomerular endothelial cells(HGEC). The aim of this study was to evaluate the expressions of VCAM-1, ICAM-1 and HLA-DR to see if there are any cytokine-dependent or time-dependent differences. METHODS: HGEC were isolated and cultured from the normal portion of the kidneys removed due to renal cell carcinoma, which was confirmed by factor VIII and fluorescent-labeled acetylated LDL. The effects of cytokine on the cell surface expression of VCAM-1, ICAM-1 and HLA-DR were measured by ELISA. RESULTS: ICAM-1 was increased by IL-1 beta, TNF-alpha and IFN-gamma. VCAM-1 was increased by IL-1 beta and TNF-alpha, not by IFN-gamma. IFN-gamma only increased expression of HLA-DR. Basal expression of ICAM-1 was higher than VCAM-1 and HLA-DR. The time course of expression was different according to adhesion molecule. CONCLUSIONS: These data showed that the expression of adhesion molecules and HLA-DR in HGEC were regulated differentially by inflammatory and immune-regulatory cytokines.
