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本文引用的文献

1
Vascular endothelial growth factor stimulates organ-specific host matrix metalloproteinase-9 expression and ovarian cancer invasion.血管内皮生长因子刺激器官特异性宿主基质金属蛋白酶-9的表达及卵巢癌侵袭。
Mol Cancer Res. 2008 Apr;6(4):525-34. doi: 10.1158/1541-7786.MCR-07-0366.
2
HIF1alpha induces the recruitment of bone marrow-derived vascular modulatory cells to regulate tumor angiogenesis and invasion.缺氧诱导因子1α(HIF1α)诱导骨髓来源的血管调节细胞募集,以调节肿瘤血管生成和侵袭。
Cancer Cell. 2008 Mar;13(3):206-20. doi: 10.1016/j.ccr.2008.01.034.
3
Matrix metalloproteinase-9 is required for tumor vasculogenesis but not for angiogenesis: role of bone marrow-derived myelomonocytic cells.基质金属蛋白酶-9是肿瘤血管生成所必需的,但不是血管新生所必需的:骨髓来源的髓单核细胞的作用。
Cancer Cell. 2008 Mar;13(3):193-205. doi: 10.1016/j.ccr.2007.11.032.
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Growth factor gradients in vascular patterning.血管形成中的生长因子梯度
Novartis Found Symp. 2007;283:194-201; discussion 201-6, 238-41. doi: 10.1002/9780470319413.ch15.
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RNA interference inhibition of matrix metalloproteinase-1 prevents melanoma metastasis by reducing tumor collagenase activity and angiogenesis.RNA干扰抑制基质金属蛋白酶-1可通过降低肿瘤胶原酶活性和血管生成来预防黑色素瘤转移。
Cancer Res. 2007 Nov 15;67(22):10849-58. doi: 10.1158/0008-5472.CAN-07-1791.
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The mouse cornea micropocket angiogenesis assay.小鼠角膜微袋血管生成试验。
Nat Protoc. 2007;2(10):2545-50. doi: 10.1038/nprot.2007.368.
7
Positive feedback regulation between MMP-9 and VEGF in human RPE cells.人视网膜色素上皮细胞中基质金属蛋白酶-9(MMP-9)与血管内皮生长因子(VEGF)之间的正反馈调节
Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4360-7. doi: 10.1167/iovs.06-1234.
8
Corneal angiogenic privilege: angiogenic and antiangiogenic factors in corneal avascularity, vasculogenesis, and wound healing (an American Ophthalmological Society thesis).角膜血管生成特权:角膜无血管状态、血管生成及伤口愈合中的血管生成和抗血管生成因子(美国眼科学会论文)
Trans Am Ophthalmol Soc. 2006;104:264-302.
9
Dexamethasone treatment and ICAM-1 deficiency impair VEGF-induced angiogenesis in adult brain.地塞米松治疗和细胞间黏附分子-1缺乏会损害成年大脑中血管内皮生长因子诱导的血管生成。
J Vasc Res. 2007;44(4):283-91. doi: 10.1159/000101450. Epub 2007 Mar 30.
10
Matrix metalloproteinases as valid clinical targets.基质金属蛋白酶作为有效的临床靶点。
Curr Pharm Des. 2007;13(3):333-46. doi: 10.2174/138161207779313551.

血管内皮生长因子与基质金属蛋白酶在体内诱导新生血管中的相互作用。

Cross-talk between vascular endothelial growth factor and matrix metalloproteinases in the induction of neovascularization in vivo.

机构信息

Department of Ophthalmology, Cole Eye Institute, Cleveland Clinic Lerner College of Medicine, Cleveland, OH 44195, USA.

出版信息

Am J Pathol. 2010 Jan;176(1):496-503. doi: 10.2353/ajpath.2010.080642. Epub 2009 Nov 30.

DOI:10.2353/ajpath.2010.080642
PMID:19948826
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2797907/
Abstract

Matrix metalloproteinases (MMPs), a specialized group of enzymes capable of proteolytically degrading extracellular matrix proteins, have been postulated to play an important role in angiogenesis. It has been suggested that MMPs can regulate neovascularization using mechanisms other than simple remodeling of the capillary basement membrane. To determine the interplay between vascular endothelial growth factor (VEGF) and MMPs, we investigated the induction of angiogenesis by recombinant active MMPs and VEGF in vivo. Using a rat corneal micropocket in vivo angiogenesis assay, we observed that the active form of MMP-9 could induce neovascularization in vivo when compared with the pro- form of the enzyme as a control. This angiogenic response could be inhibited by neutralizing VEGF antibody, which suggests that MMPs acts upstream of VEGF. Additional in vitro studies using extracellular matrix loaded with radiolabeled VEGF determined that active MMPs can enzymatically release sequestered VEGF. Interestingly, in vivo angiogenesis induced by VEGF could be inhibited by MMP inhibitors, indicating that MMPs also act downstream of VEGF. In addition, inflammation plays an important role in the induction of angiogenesis mediated by both VEGF and MMPs. Our results suggest that MMPs act both upstream and downstream of VEGF and imply that potential combination therapies of VEGF and MMP inhibitors may be a useful therapeutic approach in diseases of pathological neovascularization.

摘要

基质金属蛋白酶(MMPs)是一类能够特异性降解细胞外基质蛋白的酶,它们被认为在血管生成中发挥重要作用。有观点认为,MMPs 可以通过除简单重塑毛细血管基底膜以外的机制来调节新血管生成。为了确定血管内皮生长因子(VEGF)和 MMPs 之间的相互作用,我们研究了重组活性 MMPs 和 VEGF 在体内诱导血管生成的情况。我们利用大鼠角膜微囊体内血管生成试验发现,与作为对照的酶的前体形式相比,活性 MMP-9 形式可以在体内诱导新血管生成。这种血管生成反应可以被中和 VEGF 的抗体抑制,这表明 MMPs 在 VEGF 之前起作用。使用加载放射性标记的 VEGF 的细胞外基质进行的额外体外研究表明,活性 MMPs 可以酶解释放隔离的 VEGF。有趣的是,VEGF 诱导的体内血管生成可以被 MMP 抑制剂抑制,这表明 MMPs 也在 VEGF 之后起作用。此外,炎症在 VEGF 和 MMPs 介导的血管生成诱导中起着重要作用。我们的结果表明,MMPs 在 VEGF 的上游和下游都起作用,并暗示 VEGF 和 MMP 抑制剂的潜在联合治疗可能是病理性新生血管疾病的一种有用的治疗方法。