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Titolo:
Rhodostomin, a snake venom disintegrin, inhibits angiogenesis elicited by basic fibroblast growth factor and suppresses tumor growth by a selective alpha(v)beta(3) blockade of endothelial cells
Autore:
Yeh, CH; Peng, HC; Yang, RS; Huang, TF;
Indirizzi:
Natl Taiwan Univ, Coll Med, Dept Pharmacol, Taipei, Taiwan Natl Taiwan Univ Taipei Taiwan Coll Med, Dept Pharmacol, Taipei, Taiwan Natl Taiwan Univ, Coll Med, Dept Orthoped, Taipei, Taiwan Natl Taiwan Univ Taipei Taiwan Coll Med, Dept Orthoped, Taipei, Taiwan
Titolo Testata:
MOLECULAR PHARMACOLOGY
fascicolo: 5, volume: 59, anno: 2001,
pagine: 1333 - 1342
SICI:
0026-895X(200105)59:5<1333:RASVDI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALPHA-V INTEGRINS; IN-VIVO; ANTIANGIOGENIC AGENTS; ADHESION; APOPTOSIS; MELANOMA; ANTAGONISTS; ACTIVATION; MECHANISMS; PEPTIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Huang, TF Natl Taiwan Univ, Coll Med, Dept Pharmacol, 1,Sec 1,Jen Ai Rd, Taipei, Taiwan Natl Taiwan Univ 1,Sec 1,Jen Ai Rd Taipei Taiwan aipei, Taiwan
Citazione:
C.H. Yeh et al., "Rhodostomin, a snake venom disintegrin, inhibits angiogenesis elicited by basic fibroblast growth factor and suppresses tumor growth by a selective alpha(v)beta(3) blockade of endothelial cells", MOLEC PHARM, 59(5), 2001, pp. 1333-1342

Abstract

Angiogenesis consists of the proliferation, migration, and differentiationof endothelial cells, although angiogenic factor and integrin-extracellular matrix interaction modulate this process. We report here that a snake venom-derived disintegrin, rhodostomin, inhibited distinct steps in angiogenesis elicited by basic fibroblast growth factor (bFGF), and also suppressed in vivo murine melanoma tumor growth. Rhodostomin dose-dependently inhibitedbFGF-induced human umbilical vein endothelial cell (HUVEC) proliferation as examined by cell number count, metabolic activity, and BrdU incorporationassays with submicromolar IC50 values. However, it apparently did not affect the viability of murine B16F10 melanoma cells, even up to 50 muM. Rhodostomin also inhibited HUVEC migration and invasion evoked by bFGF, and tube formation of bFGF-treated HUVECs in Matrigel. Moreover, rhodostomin selectively inhibited bFGF-, but not vascular endothelial growth factor-associatedangiogenesis in the chick chorioallantoic membrane model. Furthermore, rhodostomin blocked both bFGF- and B16F10-induced neovascularization in murineMatrigel plug model and suppressed the growth of subcutaneously inoculatedB16F10 solid tumor, leading to a prolonged survival of the rhodostomin-treated C57BL/6 mice. The antiangiogenic effect of rhodostomin on bFGF- treated HUVECs is related to the integrin alpha (v)beta (3) blockade, as evidenced by its selective inhibition on the binding of 7E3, a monoclonal antibody (mAb) raised against alpha (v)beta (3), but not that of P1F6, an alpha (v)beta 5 mAb toward both naive and bFGF- primed HUVECs. Moreover, 7E3 specifically blocked fluorescein isothiocyanate-conjugated rhodostomin binding to HUVEC, whereas P1F6 and anti-integrin alpha (2), alpha (3), alpha (4), or alpha (5) mAbs did not.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 04:27:21