Effect of Transforming Growth Factor-beta1 (TGF-beta1) on the Expression of Vascular cell Adhesion Molecule-1 (VCAM-1) in Cultured Human Peritoneal Mesothelial Cells (HPMCs).
- Author:
Hae Hyuk JUNG
1
;
Won Seok YANG
;
Soon Bae KIM
;
Byung Sik KIM
;
Su Kil PARK
;
Jung Sik PARK
Author Information
1. Department of Internal Medicine, Kangwon National University, Korea.
- Publication Type:Original Article
- Keywords:
Peritoneal mesothelial cell;
Transforming growth factor-beta1;
Vascular cell adhesion molecule-1
- MeSH:
Blotting, Northern;
Blotting, Western;
Dactinomycin;
Enzyme-Linked Immunosorbent Assay;
Humans*;
Neutrophils;
Peritoneal Cavity;
Peritonitis;
RNA Stability;
RNA, Messenger;
Transforming Growth Factor beta1;
Tumor Necrosis Factor-alpha;
Vascular Cell Adhesion Molecule-1*
- From:Korean Journal of Nephrology
2002;21(6):956-965
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: In early phase of peritonitis, mononuclear cells as well as polymorphonuclear leukocytes migrate rapidly into peritoneal cavity. For the migration of mononuclear cells, the expression of VCAM-1 on peritoneal mesothelial cells is important. In this study, we investigated the effect of TGF-beta1 on tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta(IL-1beta) induced VCAM-1 expression in the cultured HPMCs. METHODS: HPMCs were cultured in the presence of TNF-alpha, IL-1beta and/or TGF-beta1. VCAM-1 mRNA level was measured by Northern blot. VCAM-1 in total cell lysate and VCAM-1 expressed on cell surface were measured by Western blot and cellular ELISA, respectively. RESULTS: Incubation of the cultured HPMCs with TNF-alpha (10 ng/mL) or IL-1beta (1 ng/mL) caused an increased level of VCAM-1 mRNA, VCAM-1 protein in total cell lysate, and VCAM-1 expressed on cell surface. This stimulatory effects of TNF-alpha or IL- 1beta were inhibited by TGF-beta1 (0.1, 1, 10 ng/mL), dose-dependently. The level of VCAM-1 mRNA, VCAM-1 protein in total cell lysate, and VCAM-1 expressed on cell surface in the unstimulated cells were also inhibited by TGF-beta1 (10 ng/mL). The rate of VCAM-1 mRNA degradation after an application of actinomycin D was not affected by TGF-beta1. CONCLUSION: TGF-beta1 inhibited inflammatory cytokine induced VCAM-1 production and expression in the cultured HPMCs. Treatment of the cells with TGF-beta1 seems to suppress TNF-alpha or IL-1beta induced VCAM-1 mRNA transcription rather than decrease stabilization of VCAM-1 mRNA.
