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学科主题: 临床医学
题名:
VEGF(165)b, an inhibitory vascular endothelial growth factor splice variant: Mechanism of action, in vivo effect on angiogenesis and endogenous protein expression
作者: Woolard, J; Wang, WY; Bevan, HS; Qiu, Y; Morbidelli, L; Pritchard-Jones, RO; Cui, TG; Sugiono, M; Waine, E; Perrin, R; Foster, R; Digby-Bell, J; Shields, JD; Whittles, CE; Mushens, RE; Gillatt, DA; Ziche, M; Harper, SJ; Bates, DO
刊名: CANCER RESEARCH
发表日期: 2004-11-01
卷: 64, 期:21, 页:7822-7835
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: RENAL-CELL CARCINOMA ; PERMEABILITY FACTOR ; MESSENGER-RNA ; SIGNALING PATHWAYS ; HUMAN PODOCYTES ; FACTOR ISOFORM ; RAT MESENTERY ; FACTOR VEGF ; RECEPTORS ; CANCER
英文摘要:

Growth of new blood vessels (angiogenesis), required for all tumor growth, is stimulated by the expression of vascular endothelial growth factor (VEGF). VEGF is up-regulated in all known solid tumors but also in atherosclerosis, diabetic retinopathy, arthritis, and many other conditions. Conventional VEGF isoforms have been universally described as proangiogenic cytokines. Here, we show that an endogenous splice variant, VEGF(165)b, is expressed as protein in normal cells and tissues and is circulating in human plasma. We also present evidence for a sister family of presumably inhibitory splice variants. Moreover, these isoforms are down-regulated in prostate cancer. We also show that VEGF(165)b binds VEGF receptor 2 with the same affinity as VEGF(165) but does not activate it or stimulate downstream signaling pathways. Moreover, it prevents VEGF(165)-mediated VEGF receptor 2 phosphorylation and signaling in cultured cells. Furthermore, we show, with two different in vivo angiogenesis models, that VEGF(165)b is not angiogenic and that it inhibits VEGF(165)-mediated angiogenesis in rabbit cornea and rat mesentery. Finally, we show that VEGF(165)b expressing tumors grow significantly more slowly than VEGF(165)-expressing tumors, indicating that a switch in splicing from VEGF(165) to VEGF(165)b can inhibit tumor growth. These results suggest that regulation of VEGF splicing may be a critical switch from an antiangiogenic to a proangiogenic phenotype.

语种: 英语
WOS记录号: WOS:000224790600027
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/66265
Appears in Collections:北京大学第一临床医学院_肾脏内科_期刊论文

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作者单位: 1.Univ Siena, Pharmacol Sect, Dept Mol Biol, I-53100 Siena, Italy
2.Univ Bristol, Preclin Vet Sch, Microvasc Res Labs, Dept Physiol, Bristol BS2 8EJ, Avon, England
3.Beijing Univ, Teaching Hosp 1, Inst Nephrol, Beijing 100871, Peoples R China
4.Southmead Gen Hosp, Natl Blood Transfus Ctr, Bristol Urol Inst, Bristol, Avon, England
5.Southmead Gen Hosp, Natl Blood Transfus Ctr, Int Blood Grp Reference Labs, Bristol, Avon, England

Recommended Citation:
Woolard, J,Wang, WY,Bevan, HS,et al. VEGF(165)b, an inhibitory vascular endothelial growth factor splice variant: Mechanism of action, in vivo effect on angiogenesis and endogenous protein expression[J]. CANCER RESEARCH,2004,64(21):7822-7835.
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