Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Transcriptional regulation of the leptin gene promoter in rat GH3 pituitary and C6 glioma cells
Autore:
Li, AW; Morash, B; Hollenberg, AN; Ur, E; Wilkinson, M; Murphy, PR;
Indirizzi:
Dalhousie Univ, Fac Med, Dept Physiol & Biophys, Halifax, NS B3H 4H7, Canada Dalhousie Univ Halifax NS Canada B3H 4H7 hys, Halifax, NS B3H 4H7, Canada Dalhousie Univ, Dept Obstet & Gynaecol, Halifax, NS B3H 4H7, Canada Dalhousie Univ Halifax NS Canada B3H 4H7 col, Halifax, NS B3H 4H7, Canada Dalhousie Univ, Div Endocrinol, Halifax, NS B3H 4H7, Canada Dalhousie Univ Halifax NS Canada B3H 4H7 nol, Halifax, NS B3H 4H7, Canada Beth Israel Deaconess Med Ctr, Div Endocrinol, Boston, MA 02215 USA Beth Israel Deaconess Med Ctr Boston MA USA 02215 l, Boston, MA 02215 USA
Titolo Testata:
MOLECULAR AND CELLULAR ENDOCRINOLOGY
fascicolo: 1-2, volume: 176, anno: 2001,
pagine: 57 - 65
SICI:
0303-7207(20010515)176:1-2<57:TROTLG>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
BINDING PROTEIN-ALPHA; WHITE ADIPOSE-TISSUE; OB GENE; OBESE GENE; RECEPTOR EXPRESSION; 3T3-L1 ADIPOCYTES; BRAIN-DEVELOPMENT; MESSENGER-RNA; ACTIVATION; SECRETION;
Keywords:
leptin gene; GH3 pituitary; C6 glima cells;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Murphy, PR Dalhousie Univ, Fac Med, Dept Physiol & Biophys, Halifax, NS B3H 4H7, Canada Dalhousie Univ Halifax NS Canada B3H 4H7 x, NS B3H 4H7, Canada
Citazione:
A.W. Li et al., "Transcriptional regulation of the leptin gene promoter in rat GH3 pituitary and C6 glioma cells", MOL C ENDOC, 176(1-2), 2001, pp. 57-65

Abstract

Leptin was originally believed to be an exclusively adipocyte-derived hormone regulating appetite and energy balance. It has recently become apparentthat leptin is actively expressed in a number of other tissues including the CNS and pituitary, as well as brain- and pituitary-derived cell lines. However, the factors controlling leptin expression in cells of neuroectodermal origin are unknown. The mouse leptin gene 5'-flanking DNA contains multiple AP-I and SRF-1 binding sites as well as a consensus CRE site at -491 to-482 bp. In addition, a number of potential PIT1 and Oct-1 binding sites may contribute to leptin gene transcription in pituitary and brain. We have used leptin promoter-luciferase reporter constructs to examine the regulation of the leptin promoter in 3T3-L1 preadipocytes, C6 glioma cells, and GH3pituitary cells in response to serum and hormonal stimuli. Cells were transiently transfected with reporter constructs containing either the proximal500 bp of the leptin promoter (- 500-luc) or 6000 bp of the leptin gene 5'flanking region (- 6000-1uc). Functional analysis indicates that the leptin promoter is constitutively active in all 3 cell lines. Transcriptional activity was significantly higher with a - 500 to + 9 promoter than with a construct containing - 6000 to + 9 bp of 5' flanking DNA, indicating the presence of repressor elements which may contribute to the tissue-specific regulation of leptin expression. However, qualitatively similar results were observed with both constructs in response to serum and hormonal manipulation. Leptin promoter activity was significantly stimulated by serum in all celllines, although to varying extents. Ill contrast, the response of the leptin promoter to insulin, ICF-I and dibutyryl cAMP was cell-type specific anddependent on the presence or absence of FBS in the culture medium. Insulin, IGF-1 and dibutyryl cAMP each caused an approximately two-fold stimulation of leptin promoter activity in 3T3-L1 cells under serum-free conditions, but had no significant effect in the presence of 10% FBS. In contrast, dibutyryl cAMP markedly stimulated leptin promoter activity (5-8-fold) in C6 orGH3 cells in the presence or absence of FBS, whereas insulin or IGF-1 had minimal effects. These findings support our previous studies on the regulation of leptin steady state mRNA levels in C6 cells and demonstrate tissue-specific differences in the regulation of leptin gene transcription in adipose vs. neuroectodermal tissues. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/02/20 alle ore 07:26:44