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Tumor Necrosis Factor‐Alpha Up‐Regulates ICAM‐1 Expression and Release in Intestinal Myofibroblasts by Redox‐Dependent and ‐Independent Mechanisms
Author(s) -
Fontani Filippo,
Domazetovic Vladana,
Marcucci Tommaso,
Vincenzini Maria Teresa,
Iantomasi Teresa
Publication year - 2016
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25279
Subject(s) - tumor necrosis factor alpha , microbiology and biotechnology , chemistry , myofibroblast , redox , alpha (finance) , cancer research , biology , pathology , immunology , medicine , construct validity , nursing , organic chemistry , patient satisfaction , fibrosis
Intercellular adhesion molecule‐1 (ICAM‐1) is distributed and expressed on cell surface and is present in circulation as soluble form (sICAM‐1). Tumor necrosis factor‐alpha (TNFα) and radical oxygen species (ROS) up‐regulate the expression of ICAM‐1. This study demonstrates for the first time in 18 Co cells, a myofibroblast cell line derived from human colonic mucosa, an up‐regulation of ICAM‐1 expression and sICAM‐1 release induced by oxidative stress and TNFα stimulation. The intracellular redox state was modulated by L‐buthionine‐S,R‐sulfoximine (BSO) or N‐acetylcysteine (NAC), inhibitor and precursor respectively of GSH synthesis. ROS production increases in cells treated with BSO or TNFα, and this has been related to an up‐regulation of ICAM‐1 expression and sICAM‐1 release. The involvement of metalloproteinases in ICAM‐1 release has been demonstrated. Moreover, also expression and activation of A disintegrin and metalloproteinase 17, a membrane‐bound enzyme known as TNFα‐converting enzyme (TACE), have been related to ROS levels. This suggests the possible involvement of TACE in the cleavage of ICAM‐1 on cell surface in condition of oxidative stress. NAC down‐regulates the expression and release of ICAM‐1 as well as the expression and activation of TACE. However, in TNFα stimulated cells NAC treatment reduces only in part ICAM‐1 expression and sICAM‐1 release. Given this TNFα may also act on these events by a redox‐independent mechanism. J. Cell. Biochem. 117: 370–381, 2016. © 2015 Wiley Periodicals, Inc.