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

Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Research Abstract Details 

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  • Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Abstract Text:

    yu-rong tanYu-Rong Tan,xiao-qun qinXiao-Qun Qin,cha-xiang guanCha-Xiang Guan,chang-qing zhangChang-Qing Zhang,zi-qiang luoZi-Qiang Luo,xiu-hong sunXiu-Hong Sun,

    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 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-kappaB in O3-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.

    Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Publishing Authors By Initials

    yr tanYR Tan,xq qinXQ Qin,cx guanCX Guan,cq zhangCQ Zhang,zq luoZQ Luo,xh sunXH Sun,

    For similar abstracts research abstracts see: abstracts research

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    Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Sheng li xue bao : [Acta physiologica Sinica]

    VOLUME: 55

    Page Numbers: 121-7

    Journal Abbreviation:

    ISSN: 0371-0874

    DAY: 25

    MONTH: Apr

    YEAR: 2003

    Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Information

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    LANGUAGE: eng

    NlmUniqueID: 20730130

    Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells. Keywords Mesh Terms:

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    Grant and Affiliation Information for Regulatory peptides modulate ICAM-1 gene expression and NF-kappaB activity in bronchial epithelial cells.

    AFFILIATION: Department of Physiology, Xiangya School of Medicine, Central South University, Changsha 410078; E-mail: ttyyrr3668@sohu.com

    Country: China

    China Research PublicationChina Research Publication

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    MEDLINETA: Sheng Li Xue Bao

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