Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Transforming growth factor-beta 1 induces transforming growth factor-beta 1 and transforming growth factor-beta receptor messenger RNAs and reduces complement C1qB messenger RNA in rat brain microglia
Autore:
Morgan, TE; Rozovsky, I; Sarkar, DK; Young-Chan, CS; Nichols, NR; Laping, NJ; Finch, CE;
Indirizzi:
Univ So Calif, Andrus Gerontol Ctr, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 tol Ctr, Los Angeles, CA 90089 USA Univ So Calif, Dept Biol Sci, Los Angeles, CA 90089 USA Univ So Calif LosAngeles CA USA 90089 iol Sci, Los Angeles, CA 90089 USA Rutgers State Univ, Dept Anim Sci, New Brunswick, NJ 08901 USA Rutgers State Univ New Brunswick NJ USA 08901 New Brunswick, NJ 08901 USA Penn State Univ, Patent Off, University Pk, PA 16802 USA Penn State Univ University Pk PA USA 16802 f, University Pk, PA 16802 USA Monash Univ, Dept Physiol, Monash, Vic 3800, Australia Monash Univ MonashVic Australia 3800 hysiol, Monash, Vic 3800, Australia SmithKline Beecham Pharmaceut, Renal Pharmacol, King Of Prussia, PA 19406 USA SmithKline Beecham Pharmaceut King Of Prussia PA USA 19406 , PA 19406 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 2, volume: 101, anno: 2000,
pagine: 313 - 321
SICI:
0306-4522(2000)101:2<313:TGF1IT>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; AMYLOID PRECURSOR PROTEIN; TGF-BETA; ALZHEIMERS-DISEASE; TGF-BETA-1 EXPRESSION; SYNERGISTIC ACTION; GENE-EXPRESSION; II RECEPTOR; CELL-LINES;
Keywords:
inflammation; auto-induction; perforant path transection;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Morgan, TE Univ So Calif, Andrus Gerontol Ctr, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 s Angeles, CA 90089 USA
Citazione:
T.E. Morgan et al., "Transforming growth factor-beta 1 induces transforming growth factor-beta 1 and transforming growth factor-beta receptor messenger RNAs and reduces complement C1qB messenger RNA in rat brain microglia", NEUROSCIENC, 101(2), 2000, pp. 313-321

Abstract

Transforming growth factor-beta1 is a multifunctional peptide with increased expression during Alzheimer's disease and other neurodegenerative conditions which involve inflammatory mechanisms. We examined the autoregulation of transforming growth factor-beta1 and transforming growth factor-beta receptors and the effects of transforming growth factor-beta1 on complement C1q in brains of adult Fischer 344 male rats and in primary glial cultures. Perforant path transection by entorhinal cortex lesioning was used as a model for the hippocampal deafferentation of Alzheimer's disease. In the hippocampus ipsilateral to the lesion, transforming growth factor-beta1 peptide was increased >100-fold; the messenger RNAs encoding transforming growth factor-beta1, transforming growth factor-beta type I and type II receptors were also increased, but to a smaller degree. In this acute lesion paradigm, microglia are the main cell type containing transforming growth factor-beta1, transforming growth factor-beta type I and II receptor messenger RNAs, shown by immunocytochemistry in combination with in situ hybridization. Autoregulation of the transforming growth factor-beta1 system was examined by intraventricular infusion of transforming growth factor-beta1 peptide, which increased hippocampal transforming growth factor-beta1 messenger RNA levelsin a dose-dependent fashion. Similarly, transforming,orowth factor-beta1 increased levels of transforming growth factor-beta1 messenger RNA and transforming growth factor-beta type II receptor messenger RNA (IC50, 5 pM) and increased release of transforming growth factor-beta1 peptide from primary microglia cultures. Interactions of transforming growth factor-beta1 with complement system gene expression are also indicated, because transforming growth factor-beta1 decreased C1qB messenger RNA in the cortex and hippocampus, after intraventricular infusion, and in cultured glia. These indications of autocrine regulation of transforming growth factor-beta1 in the rodentbrain support a major role of microglia in neural activities of transforming growth factor-beta1 and give a new link between transforming growth factor-beta1 and the complement system. The auto-induction of the transforming growth factor-beta1 system has implications for transgenic mice that overexpress transforming growth factor-beta1 in brain cells and for its potentialrole in amyloidogenesis. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/03/20 alle ore 13:30:29