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Titolo:
ERK activation and mitogenesis in human airway smooth muscle cells
Autore:
Lee, JH; Johnson, PRA; Roth, M; Hunt, NH; Black, JL;
Indirizzi:
Univ Sydney, Dept Pharmacol, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 rmacol, Sydney, NSW 2006, Australia Univ Sydney, Dept Pathol, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 Pathol, Sydney, NSW 2006, Australia
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
fascicolo: 5, volume: 280, anno: 2001,
pagine: L1019 - L1029
SICI:
1040-0605(200105)280:5<L1019:EAAMIH>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEDIATED DNA-SYNTHESIS; RIBOSOMAL S6 KINASE; PROTEIN-KINASE; GROWTH-FACTOR; CYCLIN D1; SIGNALING PATHWAYS; MAP KINASE; PHOSPHATIDYLINOSITOL 3-KINASE; G(1) PHASE; PROLIFERATION;
Keywords:
asthma; antisense extracellular signal-regulated kinase; p90 ribosomal S6 kinase; c-Fos; cyclin D1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Black, JL Univ Sydney, Dept Pharmacol, Sydney, NSW 2006, Australia Univ Sydney Sydney NSW Australia 2006 dney, NSW 2006, Australia
Citazione:
J.H. Lee et al., "ERK activation and mitogenesis in human airway smooth muscle cells", AM J P-LUNG, 280(5), 2001, pp. L1019-L1029

Abstract

Asthmatic airways are characterized by an increase in smooth muscle mass, due mainly to hyperplasia. Many studies suggest that extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2, respectively), one group of the mitogen-activated protein (MAP) kinase superfamily, play a key role in the signal transduction pathway leading to cell proliferation. PGE(2) and forskolin inhibited mitogen-induced ERK activation. Inhibition of MAP kinase kinases 1 and 2 (MEK1 and MEK2, respectively), which are upstream from ERK, withthe specific MEK inhibitor U-0126 blocked both cell proliferation and ERK activation. In addition, U-0126 inhibited mitogen-induced activation of p90ribosomal S6 kinase and expression of c-Fos and cyclin D1, all of which are downstream from ERK in the signaling cascade that leads to cell proliferation. Antisense oligodeoxynucleotides directed to ERK1 and -2 mRNAs reducedERK protein and cell proliferation. These results indicate that ERK is required for human airway smooth muscle cell proliferation. Thus targeting thecontrol of ERK activation may provide a new therapeutic approach for hyperplasia seen in asthma.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/08/20 alle ore 03:14:12