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Titolo:
Parathyroid-induced angiogenesis is VEGF-dependent
Autore:
Carter, WB; Uy, K; Ward, MD; Hoying, JB;
Indirizzi:
Eastern Virginia Med Sch, Dept Surg, Norfolk, VA 23501 USA Eastern Virginia Med Sch Norfolk VA USA 23501 Surg, Norfolk, VA 23501 USA Vet Adm Med Ctr, Hampton, VA USA Vet Adm Med Ctr Hampton VA USAVet Adm Med Ctr, Hampton, VA USA Univ Arizona, Arizona Res Labs, Div Biomed Engn, Tucson, AZ USA Univ Arizona Tucson AZ USA ona Res Labs, Div Biomed Engn, Tucson, AZ USA
Titolo Testata:
SURGERY
fascicolo: 3, volume: 128, anno: 2000,
pagine: 458 - 464
SICI:
0039-6060(200009)128:3<458:PAIV>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOTHELIAL GROWTH-FACTOR; TUMOR ANGIOGENESIS; TRANSGENIC MICE; EXPRESSION; TISSUE; AUTOTRANSPLANTATION; NEOVASCULARIZATION; REVASCULARIZATION; TRANSPLANTATION; ANGIOPOIETIN-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Carter, WB Univ Maryland, Dept Surg, Div Surg Oncol, 22 S Greene St,54B14,Baltimore,MD 21201 USA Univ Maryland 22 S Greene St,54B14 Baltimore MD USA21201 1 USA
Citazione:
W.B. Carter et al., "Parathyroid-induced angiogenesis is VEGF-dependent", SURGERY, 128(3), 2000, pp. 458-464

Abstract

Background. Autotransplantation of parathyroid tissue after parathyroidectomy is successful at salvaging parathyroid function. The relatively high success of parathyroid transplantation is thought to be due, in part, to the ability of parathyroid tissue to induce angiogenesis and thus recruit a newvasculature. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor produced by a number of tumors and hypoxic tissues. Using a 3-dimensional intact microvessel angiogenesis system, we evaluated the role of VEGF in the stimulation of angiogenesis by human parathyroid cells. Methods. Freshly isolated rat microvessels embedded in a 3-dimensional collagen I matrix were treated with healthy 1-mm(3) fragments of human parathyroid tissue or isolated parathyroid cells. Other gels were supplemented with VEGF(165) or FLT-1 soluble receptor fusion protein to bind VEGF. After 11clays in culture, the gels were stained with Gs-1 lectin, a marker for ratendothelium, and linear growth of the microvessels was determined by usingimage analysis. Parathyroid production of VEGF was determined with reversetranscriptase-polymerase chain reaction. Results. A significant increase in microvessel growth was seen in parathyroid coculture (8.4 +/- 1.0 mm) versus VEGF(165) supplemented gels (6.2 +/- 0.3 mm, P < .01). VEGF(165) significantly augmented parathyroid-stimulated angiogenesis (13.7 +/- 2.4 mm, P < .05 vs parathyroid alone). Using quantitative reverse transcriptase-polymerase chain reaction we identified VEGF messenger RNA (mRNA) induction within I hour of parathyroid explant, with a 12-fold inn-ease by 24 hours. Treatment of parathyroid cocultures with 0.2 mu g/mL FLT-1 soluble receptor protein completely eliminated the parathyroidinduction of angiogenesis. Conclusions. Parathyroid tissue expresses low levels of VEGF mRNA, which is significantly upregulated on explantation. Furthermore, the increased VEGF expression is essential to drive parathyroid-induced angiogenesis in our model. However; our data suggests that other parathyroid-produced factors ale involved in mediating parapathyroid-induced angiogenesis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 20:52:11