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Titolo:
Nicotine inhibition of apoptosis in murine immune cells
Autore:
Hakki, A; Pennypacker, K; Eidizadeh, S; Friedman, H; Pross, S;
Indirizzi:
Univ S Florida, Coll Med, Dept Med Microbiol & Immunol, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 icrobiol & Immunol, Tampa, FL 33612 USA Univ S Florida, Coll Med, Dept Therapeut & Pharmacol, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 rapeut & Pharmacol, Tampa, FL 33612 USA
Titolo Testata:
EXPERIMENTAL BIOLOGY AND MEDICINE
fascicolo: 10, volume: 226, anno: 2001,
pagine: 947 - 953
SICI:
1535-3702(200111)226:10<947:NIOAIM>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
LUNG-CANCER CELLS; CERVICAL-MUCUS; PROLIFERATION; DISEASE; SMOKING; DEATH; EXPRESSION; WITHDRAWAL; CASPASE-3; NEOPLASIA;
Keywords:
apoptosis; nicotine; immune; caspase-3; dexamethasone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Pross, S Univ S Florida, Coll Med, Dept Med Microbiol & Immunol, MDC-10,12901 BruceB Downs Blvd, Tampa, FL 33612 USA Univ S Florida MDC-10,12901 Bruce B Downs Blvd Tampa FL USA 33612
Citazione:
A. Hakki et al., "Nicotine inhibition of apoptosis in murine immune cells", EXP BIOL ME, 226(10), 2001, pp. 947-953

Abstract

Nicotine, the addictive component of tobacco, is thought to be at least partially responsible for the deleterious effects of smoking such as heart disease and cancer. Evidence shows that nicotine is an immunomodulator and that one of its possible mechanisms is regulation of apoptosis, or programmedcell death, in immune cells. This study examined the effects and the mechanisms of action of nicotine on dexamethasone (DEX)-induced apoptosis in murine immune cells by examining the expression of levels of the 17-kDa activecaspase-3, a marker of apoptosis. Thymocytes and splenocytes from adult BALB/c female mice were incubated with concentrations, of nicotine correlating to those found in the blood and tissue of smokers (0.01 mug/ml [0.022 muM] and 1 mug/ml [2.2 muM]), concurrently with 100 nM DEX, to induce apoptosis. Cytosolic protein fractions were analyzed by Western blotting with polyclonal antibodies that recognize the active form of caspase-3. The data showed that nicotine significantly blocked the formation of the DEX-induced 17-kDa caspase-3 subunit expression. This downregulation ranged from 65% to 100% of the active caspase-3 expressed in cultures treated with DEX alone. Addition of d-tubocurarine chloride (dTC), a general nicotinic receptor antagonist, inhibited nicotine downregulation of the DEX-induced active caspase-3 expression, providing evidence that this action of nicotine was receptor-mediated. These data support that nicotine is an important immunomodulator at the level of immune cell apoptosis, a process thought to be a contributory mechanism of autoimmunity, cardiovascular disease, and carcinogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 21:22:24