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Titolo:
Effect of preproTRH antisense on thyrotropin-releasing hormone synthesis and viability of cultured rat diencephalic neurons
Autore:
Luo, LG; Lee, SL; Lechan, RM; Jackson, IMD;
Indirizzi:
Rhode Isl Hosp, Brown Med Sch, Div Endocrinol, Providence, RI 02903 USA Rhode Isl Hosp Providence RI USA 02903 docrinol, Providence, RI 02903 USA Tufts Univ, Sch Med, New England Med Ctr, Div Endocrinol, Boston, MA 02111USA Tufts Univ Boston MA USA 02111 d Ctr, Div Endocrinol, Boston, MA 02111USA
Titolo Testata:
ENDOCRINE
fascicolo: 1, volume: 15, anno: 2001,
pagine: 79 - 85
SICI:
1355-008X(200106)15:1<79:EOPAOT>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRH GENE-EXPRESSION; PEPTIDE; BRAIN;
Keywords:
thyrotropin-releasing hormone; apoptosis; hypothalamus; neuron protection; adenovirus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Jackson, IMD Rhode Isl Hosp, Brown Med Sch, Div Endocrinol, 593 Eddy St, Providence, RI02903 USA Rhode Isl Hosp 593 Eddy St Providence RI USA 02903 I02903 USA
Citazione:
L.G. Luo et al., "Effect of preproTRH antisense on thyrotropin-releasing hormone synthesis and viability of cultured rat diencephalic neurons", ENDOCRINE, 15(1), 2001, pp. 79-85

Abstract

To investigate a possible neurotropic role for thyrotropin-releasing hormone (TRH) in the central nervous system, we used recombinant antisense TRH adenovirus (TRHav) to "knock out" TRH in cultured 17-d fetal rat diencephalon. The morphology along with beta -galactosidase (beta -gal) enzyme histochemistry (X-gal staining) and TRH content (femtomoles/well) were used to measure the effect of antisense TRH virus. Control adenovirus mediated beta -gal transfection efficiency was nearly 85%, as shown by positive X-gal staining, and was without effect on cell morphology, TRH content, or the normal response to glucocorticoid (dexamethasone) exposure with enhanced TRH expression. A significant 90% decline in TRH content as well as changes in neuronal morphology (shrunken cell bodies and short dendrites) were observed after 14 but not 7 d following TRHav treatment. The addition of synthetic TRH peptide at 2.5 muM along with TRHav, but not dexamethasone, partly prevented the morphologic changes. No morphologic changes were seen in wild-type AtT20 cells, a pituitary cell line that does not produce TRH. To investigate whether neuronal death from loss of proTRH was owing to apoptosis, neuronalDNA change by means of fluorescent dye H-33342 staining, TUNEL staining, and DNA laddering analysis was examined. Eighty to 90% positive H-33342 and TUNEL staining as well as a 180- to 200-bp DNA fragment on DNA laddering analysis were found as compared to control. These results indicate that proTRH gene expression prevents neuronal apoptosis and may play a role in neuronal development and function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 11:06:18