Different ways to antiangiogenesis by angiostatin and suramin, and quantitation of angiostatin-induced antiangiogenesis

被引:13
作者
Bahramsoltani, Mahtab [1 ]
Plendl, Johanna [1 ]
机构
[1] Free Univ Berlin, Inst Vet Anat, Berlin, Germany
关键词
angiogenesis; antiangiogenesis; in vitro; angiostatic factors; quantitation; MUSCLE-CELL PROLIFERATION; ANGIOGENESIS IN-VITRO; ENDOTHELIAL-CELLS; GROWTH-FACTOR; ANTI-ANGIOGENESIS; GRANULOSA-CELLS; ATP SYNTHASE; PHASE-II; CANCER; QUANTIFICATION;
D O I
10.1111/j.1600-0463.2007.apm_405.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Angiogenesis, i.e. sprouting of new vessels, their remodelling and regression, is a prerequisite for growth and differentiation of organs and tissues. It is involved in many pathological processes, particularly growth and metastasis of tumours. Angiostatic therapy is a promising new strategy in the treatment of cancer. Angiogenesis inhibitors could intervene in the different phases of the angiogenic cascade, i.e. migration, proliferation, differentiation and three-dimensional organisation of endothelial cells, to inhibit the generation of tumour vessels. The aim of this study was to explore whether in a previously validated in vitro model for quantitation of angiogenesis the effects of the angiostatic factors angiostatin and suramin can be investigated and quantified. Examination of angiostatin and suramin showed that angiostatin-induced antiangiogenesis resulted in inverse angiogenesis. The addition of suramin initially resulted in increased angiogenesis. However, long-term incubation ultimately led to disintegration of endothelial structures, thus establishing the angiostatic effects of suramin. Antiangiogenesis was not only quantified using the previously validated method. It also lent itself to assessment of the extent of antiangiogenesis within the various phases of the angiogenic cascade. This method may therefore be employed in trial studies of potential angiostatic substances and related cellular mechanisms.
引用
收藏
页码:30 / 46
页数:17
相关论文
共 86 条
[1]
Angiogenesis assays: A critical overview [J].
Auerbach, R ;
Lewis, R ;
Shinners, B ;
Kubai, L ;
Akhtar, N .
CLINICAL CHEMISTRY, 2003, 49 (01) :32-40
[2]
Bahramsoltani M, 2004, ALTEX-ALTERN TIEREXP, V21, P227
[3]
BAHRAMSOLTANI M, 2004, THESIS FREIE U BERLI
[4]
Banning Maggi, 2005, Br J Nurs, V14, P277
[5]
In vitro tumor angiogenesis assays: Plasminogen lysine binding site 1 inhibits in vitro tumor-induced angiogenesis [J].
Barendsz-Janson, AF ;
Griffioen, AW ;
Muller, AD ;
van Dam-Mieras, MCE ;
Hillen, HFP .
JOURNAL OF VASCULAR RESEARCH, 1998, 35 (02) :109-114
[6]
Angiogenesis inhibition by angiostatin, endostatin and TNP-470 prevents cyclophosphamide induced cystitis [J].
Beecken W.-D. ;
Engl T. ;
Blaheta R. ;
Bentas W. ;
Achilles E.-G. ;
Jonas D. ;
Shing Y. ;
Camphausen K. .
Angiogenesis, 2004, 7 (1) :69-73
[7]
A murine model of ex vivo angiogenesis using aortic disks grown in fibrin clot [J].
Berger, AC ;
Wang, XQ ;
Zalatoris, A ;
Cenna, J ;
Watson, JC .
MICROVASCULAR RESEARCH, 2004, 68 (03) :179-187
[8]
Suramin treatment of human glioma xenografts; effects on tumor vasculature and oxygenation status [J].
Bernsen, HJJA ;
Rijken, PFJW ;
Peters, JPW ;
Bakker, JH ;
Boerman, RH ;
Wesseling, P ;
van der Kogel, AJ .
JOURNAL OF NEURO-ONCOLOGY, 1999, 44 (02) :129-136
[9]
Inhibitory effect of suramin in rat models of angiogenesis in vitro and in vivo [J].
Bocci, G ;
Danesi, R ;
Benelli, U ;
Innocenti, F ;
Di Paolo, A ;
Fogli, S ;
Del Tacca, M .
CANCER CHEMOTHERAPY AND PHARMACOLOGY, 1999, 43 (03) :205-212
[10]
Vascular endothelial growth factor and diabetic retinopathy: Role of oxidative stress [J].
Caldwell, RB ;
Bartoli, M ;
Behzadian, MA ;
El-Remessy, AEB ;
Al-Shabrawey, M ;
Platt, DH ;
Liou, GI ;
Caldwell, RW .
CURRENT DRUG TARGETS, 2005, 6 (04) :511-524