Beta interferon inhibits HIV-1 Tat-induced angiogenesis:: Synergism with 13-cis retinoic acid
Beta interferon inhibits HIV-1 Tat-induced angiogenesis:: Synergism with 13-cis retinoic acid
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DOI：
10.1016/s0959-8049(97)10082-x
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发表时间：
1998-03-01
影响因子：
8.4
通讯作者：
Albini, A
中科院分区：
文献类型：
--
作者：
Iurlaro, M;Benelli, R;Albini, A
Kaposi's sarcoma (KS) is a highly angiogenic lesion which frequently presents as an aggressive form in HIV-infected male patients. We have previously shown that the HIV-1 Tat protein induces endothelial cell migration and invasion in vitro and a rapid angiogenic response in vivo, suggesting that it acts as a cofactor in epidemic KS. In this study we tested beta interferon (IFN beta) and retinoic acid (RA) for the inhibition of Tat-induced angiogenesis using in vivo and in vitro models. IFN beta, at a concentration above 2500 U/ml, was an effective inhibitor of Tat-stimulated growth, migration and morphogenesis of an endothelial cell line in vitro and of angiogenesis in vivo. A strong reduction of properties associated with neovascularisation was induced by 10000 U/ml. In vivo, RA alone was on ineffective inhibitor of angiogenesis, and in vitro gave only a limited inhibition of endothelial cell growth. However, 13-cis RA used in combination with IFN beta impressively potentiated its effects. A combination of lower doses of IFN beta (2500 U/ml) and 13-cis RA induced a virtually complete inhibition of the Tat-related angiogenic phenotype both in vivo and in vitro. The potentiation of the anti-angiogenic activity of IFN beta by 13-cis RA suggests that this combination could be a useful approach for the therapy of epidemic KS. (C) 1998 Elsevier Science Ltd. All rights reserved.
