Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells.
- Author:
Yu-Rong TAN
1
;
Xiao-Qun QIN
;
Cha-Xiang GUAN
;
Chang-Qing ZHANG
;
Zi-Qiang LUO
;
Xiu-Hong SUN
Author Information
1. Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, PR China. ttyyrr3668@sohu.com
- Publication Type:Journal Article
- MeSH:
Animals;
Bronchi;
cytology;
Cell Adhesion;
physiology;
Cells, Cultured;
Endothelin-1;
metabolism;
Epithelial Cells;
cytology;
metabolism;
Humans;
Inflammation;
metabolism;
Intercellular Adhesion Molecule-1;
metabolism;
NF-kappa B;
metabolism;
Peptides;
physiology;
Rabbits;
Vasoactive Intestinal Peptide;
physiology
- From:
Acta Physiologica Sinica
2003;55(2):121-127
- CountryChina
- Language:English
-
Abstract:
Intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule leading to adhesion between cells; NF-kappaB, being universally distributed in the organism, is an important nuclear transcription factor leading to a rapid response to the stimuli. Line of evidence have shown that ICAM-1 transcription and NF-kappaB activation is an important step of inflammatory reaction. To testify that intrapulmonary regulatory peptides modulate inflammatory lesion of bronchial epithelial cells (BECs) through their effect on ICAM-1 expression and nuclear factor kappaB (NF-kappaB) activation, we used immunocytochemistry, RT-PCR, and electrophoretic mobility-shift assay (EMSA) to determine the ICAM-1 expression and NF-kappaB activity in BECs. The effects of NF-kappaB inhibitor MG-132 on ICAM-1 expression were also observed. The results showed that vasoactive intestinal peptide (VIP) and epidermal growth factor (EGF) decreased ICAM-1 expression in O(3)-stressed BECs, while endothelin-1 (ET-1) and calcitonin gene-related peptides (CGRP) increased ICAM-1 expression in resting BECs. MG-132 blocked ICAM-1 expression induced by O(3), ET-1 and CGRP. The results obtained by using EMSA confirmed that VIP and EGF restrained the activation of NF-kappaB in O(3)-stressed BECs; CGRP and ET-1 promoted activation of NF-kappaB. These observations indicate that VIP and EGF abated the injury by means of down-regulatory effects on ICAM-1 transcription and NF-kappaB activation, while ET-1 and CGRP enhanced the inflammation reaction by an up-regulatory effect. It is suggested that a developing and intensive airway inflammation correlates closely with a persistent expression of ICAM-1 and repeated activation of NF-kappaB.
