RETRACTED: NO-mesalamine protects colonic epithelial cells against apoptotic damage induced by proinflammatory cytokines (Retracted Article. See vol 297, pg G860, 2009)

被引:18
作者
Fiorucci, S
Distrutti, E
Ajuebor, MN
Mencarelli, A
Mannucci, R
Palazzetti, B
Del Soldato, P
Morelli, A
Wallace, JL
机构
[1] Univ Perugia, Dipartimento Med Clin & Sperimentale, Clin Gastroenterol & Epatol, I-06100 Perugia, Italy
[2] Univ Perugia, Dipartimento Med Clin & Sperimentale, Sez Med Interna & Sci Oncol, I-06100 Perugia, Italy
[3] Univ Calgary, Mucosal Inflammat Res Grp, Calgary, AB T2N 4N1, Canada
[4] Nicox, F-06906 Sophia Antipolis, France
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2001年 / 281卷 / 03期
关键词
colon cancer cells; apoptosis; death factors; nitromesalamine;
D O I
10.1152/ajpgi.2001.281.3.G654
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
The activation of a self-amplifying cascade of caspases, of which caspase-8 is the apical. protease, mediates Fas-, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-, and TNF-alpha -induced apoptosis in colon cell lines. Nitric oxide (NO) protects from apoptosis induced by Fas and TNF-alpha. We examined whether NCX-456, an NO-releasing derivative of mesalamine, protects colon epithelial cells from cytokine-induced apoptosis. Caco-2 and HT-29 cell lines express death factor receptors and are driven to apoptosis in response to incubation with Fas-agonistic antibody, TNF-alpha /interferon-gamma, and TRAIL. The two novel observations reported here are that 1) cotreatment of cells with NCX-456, but not mesalamine, resulted in concentration-dependent protection against death factor-induced apoptosis and inhibition of caspase activity, and 2) exposure to dithiothreitol, an agent that effectively removes NO from thiol groups, resulted in a 70% recovery of caspase activity, which is consistent with S-nitrosation as a major mechanism for caspase inactivation. These data suggest that caspase S-nitrosation represents a mechanism for protection of colonic mucosal epithelial cells from death factor-induced death.
引用
收藏
页码:G654 / G665
页数:12
相关论文
共 40 条
[1]   Fas activates the JNK pathway in human colonic epithelial cells: lack of a direct role in apoptosis [J].
Abreu-Martin, MT ;
Palladino, AA ;
Faris, M ;
Carramanzana, NM ;
Nel, AE ;
Targan, SR .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 1999, 276 (03) :G599-G605
[2]  
ABREUMARTIN MT, 1995, J IMMUNOL, V155, P4147
[3]   Human ICE/CED-3 protease nomenclature [J].
Alnemri, ES ;
Livingston, DJ ;
Nicholson, DW ;
Salvesen, G ;
Thornberry, NA ;
Wong, WW ;
Yuan, JY .
CELL, 1996, 87 (02) :171-171
[4]   Death receptors: Signaling and modulation [J].
Ashkenazi, A ;
Dixit, VM .
SCIENCE, 1998, 281 (5381) :1305-1308
[5]   Stimulated human lamina propria T cells manifest enhanced Fas-mediated apoptosis [J].
Boirivant, M ;
Pica, R ;
DeMaria, R ;
Testi, R ;
Pallone, F ;
Strober, W .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 98 (11) :2616-2622
[6]   NITRIC-OXIDE SYNTHASE ACTIVITY IN ULCERATIVE-COLITIS AND CROHNS-DISEASE [J].
BOUGHTONSMITH, NK ;
EVANS, SM ;
HAWKEY, CJ ;
COLE, AT ;
BALSITIS, M ;
WHITTLE, BJR ;
MONCADA, S .
LANCET, 1993, 342 (8867) :338-340
[7]  
COLTON T, 1978, STAT MED
[8]   Functional expression of Fas and Fas ligand on human gut lamina propria T lymphocytes - A potential role for the acidic sphingomyelinase pathway in normal immunoregulation [J].
DeMaria, R ;
Boirivant, M ;
Cifone, MG ;
Roncaioli, P ;
Hahne, M ;
Tschopp, J ;
Pallone, F ;
Santoni, A ;
Testi, R .
JOURNAL OF CLINICAL INVESTIGATION, 1996, 97 (02) :316-322
[9]   Nitric oxide and apoptosis: Another paradigm for the double-edged role of nitric oxide [J].
Dimmeler, S ;
Zeiher, AM .
NITRIC OXIDE-BIOLOGY AND CHEMISTRY, 1997, 1 (04) :275-281
[10]   Suppression of apoptosis by nitric oxide via inhibition of interleukin-1 beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases [J].
Dimmeler, S ;
Haendeler, J ;
Nehls, M ;
Zeiher, AM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (04) :601-607