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Titolo:
Transforming growth factor-beta 1 enhances expression of brain-derived neurotrophic factor and its receptor, TrkB, in neurons cultured from rat cerebral cortex
Autore:
Sometani, A; Kataoka, H; Nitta, AI; Fukumitsu, H; Nomoto, H; Furukawa, S;
Indirizzi:
Gifu Pharmaceut Univ, Mol Biol Lab, Gifu 5028585, Japan Gifu Pharmaceut Univ Gifu Japan 5028585 ol Biol Lab, Gifu 5028585, Japan
Titolo Testata:
JOURNAL OF NEUROSCIENCE RESEARCH
fascicolo: 3, volume: 66, anno: 2001,
pagine: 369 - 376
SICI:
0360-4012(20011101)66:3<369:TGF1EE>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR MESSENGER-RNA; FACTOR-BETA; TGF-BETA; SPINAL-CORD; HIPPOCAMPAL-NEURONS; NERVOUS-SYSTEM; CELL-DEATH; BDNF; TGF-BETA-1; INJURY;
Keywords:
transforming growth factor (TGF)-beta; brain-derived neurotrophic factor (BDNF); TrkB; neurons culture;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Furukawa, S Gifu Pharmaceut Univ, Mol Biol Lab, 5-6-1 Mitahora Higashi, Gifu 5028585, Japan Gifu Pharmaceut Univ 5-6-1 Mitahora Higashi Gifu Japan 5028585
Citazione:
A. Sometani et al., "Transforming growth factor-beta 1 enhances expression of brain-derived neurotrophic factor and its receptor, TrkB, in neurons cultured from rat cerebral cortex", J NEUROSC R, 66(3), 2001, pp. 369-376

Abstract

The effects of transforming growth factor (TGF)-beta1 on expression of brain-derived neurotrophic factor (BDNF) and Its high-affinity receptor, TrkB,in neurons cultured from the cerebral cortex of 18-day-old embryonic rats were examined. BDNF mRNA was significantly increased from 24-48 hr after the TGF-beta1 treatment over 20 ng/ml. Accumulation of BDNF protein in the culture medium was also potentiated by TGF-beta1, although the intracellular content of BDNF was nearly unchanged. The enhancement of BDNF mRNA expression was suppressed by the co-presence of decorin, a small TGF-beta -binding proteoglycan that inhibits the biological activities of TGF-betas. mRNA expression of full-length TrkB, the bioactive high-affinity receptor for BDNF,was also upregulated after treatment with TGF-beta1. These observations suggest that: 1) TGF-beta1 potentiates BDNF/TrkB autocrine or local paracrinesystem; and 2) the neurotrophic activity of TGF-beta1 is partly responsible for the BDNF induced by TGF-beta1 itself. To test this latter possibility, we examined the neuronal survival activity of TGF-beta1 with or without K252a, a selective inhibitor of Trk family tyrosine kinases. TGF-beta1 significantly enhanced neuronal survival, but the co-presence of K252a completely suppressed the activity, demonstrating the involvement of Trk receptor signaling in TGF-beta1-mediated neuronal survival in cultured rat cortical neurons. These results seem to be In line with recent findings by other investigators that some neurotrophic factors including BDNF require TGF-betas asa cofactor to exert their neurotrophic activities. (C) 2001 Wiley-Liss, inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 19:37:04