Regulatory peptides modulate ICAM-1 gene expression and NF-κB activity in bronchial epithelial cells

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TAN Yu-rong()
QIN Xiao-Qun()
GUAN Cha-Xiang()
ZHANG Chang-Qing()
LUO Zi-qiang()
SUN Xiu-Hong()
Journal Title:
Volume 55, Issue 02, 2003
Key Word:
intrapulmonary regulatory peptides;intercellular adhesion molecule-1 (ICAM-1);nuclear factor κB (NF-κB);bronchial epithelial cells

Abstract: Intercellular adhesion molecule-1 (ICAM-1) is an important adhesion molecule leading to adhesion between cells; NF-ΚB, 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-ΚB 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 ΚB (NF-ΚB) activation, we used immunocytochemistry, RT-PCR, and electrophoretic mobility-shift assay (EMSA) to determine the ICAM-1 expression and NF-ΚB activity in BECs. The effects of NF-ΚB 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 O3-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 O3, ET-1 and CGRP. The results obtained by using EMSA confirmed that VIP and EGF restrained the activation of NF-ΚB in O3-stressed BECs; CGRP and ET-1 promoted activation of NF-ΚB. These observations indicate that VIP and EGF abated the injury by means of down-regulatory effects on ICAM-1 transcription and NF-ΚB 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-ΚB.

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