Tumor Necrosis Factor-Alpha Up-Regulates ICAM-1 Expression and Release in Intestinal Myofibroblasts by Redox-Dependent and -Independent Mechanisms

Journal of Cellular BiochemistryVolume 117, Issue 2 p. 370-381 Article Tumor Necrosis Factor-Alpha Up-Regulates ICAM-1 Expression and Release in Intestinal Myofibroblasts by Redox-Dependent and -Independent Mechanisms Filippo Fontani, Filippo Fontani Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorVladana Domazetovic, Vladana Domazetovic Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorTommaso Marcucci, Tommaso Marcucci Santa Maria Annunziata Hospital, Section of General Surgery, 50126 Via dell'Antella 58, Ponte a Niccheri (Florence), ItalySearch for more papers by this authorMaria Teresa Vincenzini, Maria Teresa Vincenzini Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorTeresa Iantomasi, Corresponding Author Teresa Iantomasi Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, Italy Correspondence to: Teresa Iantomasi, Department of Biomedical, Experimental and Clinical Sciences "Mario Serio" Viale Morgagni 50, 50134 Firenze. E-mail: tiantomasi@unifi.itSearch for more papers by this author Filippo Fontani, Filippo Fontani Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorVladana Domazetovic, Vladana Domazetovic Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorTommaso Marcucci, Tommaso Marcucci Santa Maria Annunziata Hospital, Section of General Surgery, 50126 Via dell'Antella 58, Ponte a Niccheri (Florence), ItalySearch for more papers by this authorMaria Teresa Vincenzini, Maria Teresa Vincenzini Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, ItalySearch for more papers by this authorTeresa Iantomasi, Corresponding Author Teresa Iantomasi Department of Biomedical, Experimental and Clinical Sciences "Mario Serio", University of Florence, Viale Morgagni 50, 50134 Florence, Italy Correspondence to: Teresa Iantomasi, Department of Biomedical, Experimental and Clinical Sciences "Mario Serio" Viale Morgagni 50, 50134 Firenze. E-mail: tiantomasi@unifi.itSearch for more papers by this author First published: 14 July 2015 https://doi.org/10.1002/jcb.25279Citations: 9 Conflicts of interest: The authors have not conflict of interest. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat ABSTRACT 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. Citing Literature Volume117, Issue2February 2016Pages 370-381 RelatedInformation