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Titolo:
Hypoxia increases thrombospondin-1 transcript and protein in cultured endothelial cells
Autore:
Phelan, MW; Forman, LW; Perrine, SP; Faller, DV;
Indirizzi:
Boston Univ, Sch Med, Canc Res Ctr, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 h Med, Canc Res Ctr, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Med, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 , Sch Med, Dept Med, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Biochem, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 h Med, Dept Biochem, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Pediat, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 ch Med, Dept Pediat, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Microbiol, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 Med, Dept Microbiol, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Pathol, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 ch Med, Dept Pathol, Boston, MA 02118 USA Boston Univ, Sch Med, Dept Lab Med, Boston, MA 02118 USA Boston Univ Boston MA USA 02118 h Med, Dept Lab Med, Boston, MA 02118 USA
Titolo Testata:
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
fascicolo: 6, volume: 132, anno: 1998,
pagine: 519 - 529
SICI:
0022-2143(199812)132:6<519:HITTAP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
THROMBIN-SENSITIVE PROTEIN; OVARIAN-CARCINOMA CELLS; MURINE TUMOR-CELLS; GROWTH-FACTOR; SODIUM-BUTYRATE; MESSENGER-RNA; GENE-EXPRESSION; LFA-1-DEPENDENT MECHANISM; PULMONARY-HYPERTENSION; EXTRACELLULAR-MATRIX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
85
Recensione:
Indirizzi per estratti:
Indirizzo: Faller, DV Boston Univ, Sch Med, Canc Res Ctr, K-701,80 E Concord St, Boston, MA 02118 Boston Univ K-701,80 E Concord St Boston MA USA 02118 MA 02118
Citazione:
M.W. Phelan et al., "Hypoxia increases thrombospondin-1 transcript and protein in cultured endothelial cells", J LA CL MED, 132(6), 1998, pp. 519-529

Abstract

The exposure of endothelial cells to hypoxic environments regulates the expression of a number of genes with products that are vasoactive or mitogenic for vascular tissue, including platelet-derived growth factor, endothelin-1, and endothelial nitric oxide synthase. Hypoxia is also known to alter the adhesive properties of endothelium toward a variety of blood cell types. Thrombospondin-1 (TSP-1) is a glycoprotein with major roles in cellular adhesion and vascular smooth muscle proliferation and migration. We report here that hypoxia induces TSP-1 gene and protein expression. Oxygen tensions of less than or equal to 30 torr resulted in TSP-1 transcript induction initially apparent at 1 to 6 hours, with maximal induction (6.5-fold +/- 1.2-fold) within 24 to 48 hours in both human and bovine endothelial cells. TSP-1 protein levels remain elevated after 72 hours of continuous hypoxic exposure. The induction of TSP-1 steady-state transcript levels is caused in large part, if not entirely by post-transcriptional stabilization of the TSP-1mRNA. The TSP-1 induction by hypoxia is a graded and reversible physiologic response and can be mimicked by the use of cobalt chloride or the inhibition of nitric oxide production, suggesting both the involvement of a heme-containing oxygen sensor and a role for the endogenous production of nitric oxide in TSP-1 regulation. The effects of hypoxia both on the stabilizationof the TSP-1 transcript and the stimulation of TSP-1 protein production are completely inhibited by arginine butyrate.

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Documento generato il 23/09/20 alle ore 16:10:50