Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice
SUMMARY 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 β3-integrins support enhanced tumour angiogenesis and, therefore, deletion of endothelial αvβ...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
The Company of Biologists
2013-01-01
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| Series: | Disease Models & Mechanisms |
| Online Access: | http://dmm.biologists.org/content/6/1/115 |
| _version_ | 1818014397607444480 |
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| author | Dylan T. Jones Tanguy Lechertier Louise E. Reynolds Richard Mitter Stephen D. Robinson Catherine B. Kirn-Safran Kairbaan M. Hodivala-Dilke |
| author_facet | Dylan T. Jones Tanguy Lechertier Louise E. Reynolds Richard Mitter Stephen D. Robinson Catherine B. Kirn-Safran Kairbaan M. Hodivala-Dilke |
| author_sort | Dylan T. Jones |
| collection | DOAJ |
| description | SUMMARY
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 β3-integrins support enhanced tumour angiogenesis and, therefore, deletion of endothelial αvβ3 can provide a method for discovery of novel regulators of tumour angiogenesis. Here, we describe significant upregulation of RPL29 in β3-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. |
| first_indexed | 2024-04-14T06:45:02Z |
| format | Article |
| id | doaj.art-bcdc0562099e4d4baa6877853fc23d6f |
| institution | Directory Open Access Journal |
| issn | 1754-8403 1754-8411 |
| language | English |
| last_indexed | 2024-04-14T06:45:02Z |
| publishDate | 2013-01-01 |
| publisher | The Company of Biologists |
| record_format | Article |
| series | Disease Models & Mechanisms |
| spelling | doaj.art-bcdc0562099e4d4baa6877853fc23d6f2022-12-22T02:07:13ZengThe Company of BiologistsDisease Models & Mechanisms1754-84031754-84112013-01-016111512410.1242/dmm.009183009183Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in miceDylan T. JonesTanguy LechertierLouise E. ReynoldsRichard MitterStephen D. RobinsonCatherine B. Kirn-SafranKairbaan M. Hodivala-DilkeSUMMARY 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 β3-integrins support enhanced tumour angiogenesis and, therefore, deletion of endothelial αvβ3 can provide a method for discovery of novel regulators of tumour angiogenesis. Here, we describe significant upregulation of RPL29 in β3-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.http://dmm.biologists.org/content/6/1/115 |
| spellingShingle | Dylan T. Jones Tanguy Lechertier Louise E. Reynolds Richard Mitter Stephen D. Robinson Catherine B. Kirn-Safran Kairbaan M. Hodivala-Dilke Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice Disease Models & Mechanisms |
| title | Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice |
| title_full | Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice |
| title_fullStr | Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice |
| title_full_unstemmed | Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice |
| title_short | Endogenous ribosomal protein L29 (RPL29): a newly identified regulator of angiogenesis in mice |
| title_sort | endogenous ribosomal protein l29 rpl29 a newly identified regulator of angiogenesis in mice |
| url | http://dmm.biologists.org/content/6/1/115 |
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