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Titolo:
Activation of mitogen-activated protein kinases is required for alpha(1)-adrenergic agonist-induced cell scattering in transfected HepG2 cells
Autore:
Spector, M; Nguyen, VA; Sheng, XN; He, LS; Woodward, J; Fan, SJ; Baumgarten, CM; Kunos, G; Dent, P; Gao, B;
Indirizzi:
Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA Virginia Commonwealth Univ, Med Coll Virginia, Dept Physiol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA Virginia Commonwealth Univ, Med Coll Virginia, Dept Radiat Oncol, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA NCI, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892NCI, NIH, Bethesda, MD 20892 USA Albert Einstein Coll Med, Long Isl Jewish Med Ctr, Dept Radiat Oncol, New York, NY USA Albert Einstein Coll Med New York NY USA Radiat Oncol, New York, NY USA
Titolo Testata:
EXPERIMENTAL CELL RESEARCH
fascicolo: 1, volume: 258, anno: 2000,
pagine: 109 - 120
SICI:
0014-4827(20000710)258:1<109:AOMPKI>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEPATOCYTE GROWTH-FACTOR; CARDIAC MYOCYTE HYPERTROPHY; GENE-EXPRESSION; PHOSPHATIDYLINOSITOL 3-KINASE; ADRENERGIC-RECEPTORS; SIGNALING PATHWAY; RAT HEPATOCYTES; SMOOTH-MUSCLE; MAP KINASE; BETA-2-ADRENERGIC RECEPTORS;
Keywords:
cell hypertrophy; protein kinase C; AP1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Gao, B Virginia Commonwealth Univ, Med Coll Virginia, Dept Pharmacol & Toxicol, Box 980613, Richmond, VA 23298 USA Virginia Commonwealth Univ Box 980613 Richmond VA USA 23298 298 USA
Citazione:
M. Spector et al., "Activation of mitogen-activated protein kinases is required for alpha(1)-adrenergic agonist-induced cell scattering in transfected HepG2 cells", EXP CELL RE, 258(1), 2000, pp. 109-120

Abstract

Activation of alpha(1B)-adrenergic receptors (alpha(1B)AR) by phenylephrine (PE) induces scattering of HepG2 cells stably transfected with the alpha(1B)AR (TFG2 cells). Scattering was also observed after stimulation of TFG2 cells with phorbol myristate acetate (PMA) but not with hepatocyte growth factor/scatter factor, epidermal growth factor, or insulin. PMA but not phenylephrine rapidly activated PKC alpha in TFG2 cells, and the highly selective PKC inhibitor bisindolylmaleimide (GFX) completely abolished PMA-inducedbut not PE-induced scattering PE rapidly activated p44/42 mitogen-activated protein kinase (MAPK), p38 MAPK, c-Jun N-terminal kinase (JNK), and AP1 (c-fos/c-jun), Selective blockade of p42/44 MAPK activity by PD98059 or by transfection of a MEK1 dominant negative adenovirus significantly inhibited the PE-induced scattering of TFG2 cells. Selective inhibition of p38 MAPK by SB203850 or SB202190 also blocked PE-induced scattering, whereas treatment of TFG2 cells with the PI3 kinase inhibitors LY294002 or wortmannin did not inhibit PE-induced scattering. Blocking JNK activation with a dominant negative mutant of JNK or blocking AP1 activation with a dominant negative mutant of c-jun (TAM67) significantly inhibited PE-induced cell scattering These data indicate that PE-induced scattering of TFG2 cells is mediated by complex mechanisms, including activation of p42/44 MAPK, p38 MAPK, and JNK,Cell spreading has been reported to play important roles in wound repair, tumor invasion, and metastasis, Therefore, catecholamines acting via the alpha(1)AR may modulate these physiological and pathological processes. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 22:56:19