期刊
DISEASE MODELS & MECHANISMS
卷 6, 期 1, 页码 115-124出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/dmm.009183
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资金
- Breast Cancer Campaign [BCC 2008 MayPR07]
- Cancer Research UK [CRUK C8212_A12007]
- National Institutes of Health [P20-RR016458]
- CRUK
- MRC [G0901609] Funding Source: UKRI
- Cancer Research UK [12007] Funding Source: researchfish
- Medical Research Council [1365527, G0901609] Funding Source: researchfish
- Worldwide Cancer Research [12-1068] Funding Source: researchfish
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016458] Funding Source: NIH RePORTER
Cellular ribosomal protein L29 (RPL29) is known to be important in protein synthesis, but its function during angiogenesis has never been described before. We have shown previously that mice lacking. 3-integrins support enhanced tumour angiogenesis and, therefore, deletion of endothelial. v. 3 can provide a method for discovery of novel regulators of tumour angiogenesis. Here, we describe significant upregulation of RPL29 in beta 3-null endothelial cells at both the mRNA and protein level. Ex vivo, we show that VEGF-stimulated microvessel sprouting was reduced significantly in Rpl29-heterozygous and Rpl29-null aortic ring assays compared with wild-type controls. Moreover, we provide in vivo evidence that RPL29 can regulate tumour angiogenesis. Tumour blood vessel density in subcutaneously grown Lewis lung carcinomas was reduced significantly in Rpl29-mutant mice. Additionally, depletion of Rpl29 using RNA interference inhibited VEGF-induced aortic ring sprouting, suggesting that anti-RPL29 strategies might have anti-angiogenic potential. Overall, our results identify that loss or depletion of RPL29 can reduce angiogenesis in vivo and ex vivo.
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