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VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis

Vascular endothelial growth factor B (VEGF-B) was discovered a long time ago. However, its role in hyperglycemia- and VEGF-A inhibition-induced retinal apoptosis remains unknown thus far. Yet, drugs that can block VEGF-B are being used to treat patients with diabetic retinopathy and other ocular neo...

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Autores principales: Huang, Delong, Zhao, Chen, Ju, Rong, Kumar, Anil, Tian, Geng, Huang, Lijuan, Zheng, Lei, Li, Xianglin, Liu, Lixian, Wang, Shasha, Ren, Xiangrong, Ye, Zhimin, Chen, Wei, Xing, Liying, Chen, Qishan, Gao, Zhiqin, Mi, Jia, Tang, Zhongshu, Wang, Bin, Zhang, Shuping, Lee, Chunsik, Li, Xuri
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870690/
https://www.ncbi.nlm.nih.gov/pubmed/27189805
http://dx.doi.org/10.1038/srep26059
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author Huang, Delong
Zhao, Chen
Ju, Rong
Kumar, Anil
Tian, Geng
Huang, Lijuan
Zheng, Lei
Li, Xianglin
Liu, Lixian
Wang, Shasha
Ren, Xiangrong
Ye, Zhimin
Chen, Wei
Xing, Liying
Chen, Qishan
Gao, Zhiqin
Mi, Jia
Tang, Zhongshu
Wang, Bin
Zhang, Shuping
Lee, Chunsik
Li, Xuri
author_facet Huang, Delong
Zhao, Chen
Ju, Rong
Kumar, Anil
Tian, Geng
Huang, Lijuan
Zheng, Lei
Li, Xianglin
Liu, Lixian
Wang, Shasha
Ren, Xiangrong
Ye, Zhimin
Chen, Wei
Xing, Liying
Chen, Qishan
Gao, Zhiqin
Mi, Jia
Tang, Zhongshu
Wang, Bin
Zhang, Shuping
Lee, Chunsik
Li, Xuri
author_sort Huang, Delong
collection PubMed
description Vascular endothelial growth factor B (VEGF-B) was discovered a long time ago. However, its role in hyperglycemia- and VEGF-A inhibition-induced retinal apoptosis remains unknown thus far. Yet, drugs that can block VEGF-B are being used to treat patients with diabetic retinopathy and other ocular neovascular diseases. It is therefore urgent to have a better understanding of the function of VEGF-B in these pathologies. Here, we report that both streptozotocin (STZ)-induced diabetes in rats and Macugen intravitreal injection in mice leads to retinal apoptosis in retinal ganglion cell and outer nuclear layers respectively. Importantly, VEGF-B treatment by intravitreal injection markedly reduced retinal apoptosis in both models. We further reveal that VEGF-B and its receptors, vascular endothelial growth factor 1 (VEGFR1) and neuropilin 1 (NP1), are abundantly expressed in rat retinae and choroids and are upregulated by high glucose with concomitant activation of Akt and Erk. These data highlight an important function of VEGF-B in protecting retinal cells from apoptosis induced by hyperglycemia and VEGF-A inhibition. VEGF-B may therefore have a therapeutic potential in treating various retinal degenerative diseases, and modulation of VEGF-B activity in the eye needs careful consideration.
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spelling pubmed-48706902016-06-01 VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis Huang, Delong Zhao, Chen Ju, Rong Kumar, Anil Tian, Geng Huang, Lijuan Zheng, Lei Li, Xianglin Liu, Lixian Wang, Shasha Ren, Xiangrong Ye, Zhimin Chen, Wei Xing, Liying Chen, Qishan Gao, Zhiqin Mi, Jia Tang, Zhongshu Wang, Bin Zhang, Shuping Lee, Chunsik Li, Xuri Sci Rep Article Vascular endothelial growth factor B (VEGF-B) was discovered a long time ago. However, its role in hyperglycemia- and VEGF-A inhibition-induced retinal apoptosis remains unknown thus far. Yet, drugs that can block VEGF-B are being used to treat patients with diabetic retinopathy and other ocular neovascular diseases. It is therefore urgent to have a better understanding of the function of VEGF-B in these pathologies. Here, we report that both streptozotocin (STZ)-induced diabetes in rats and Macugen intravitreal injection in mice leads to retinal apoptosis in retinal ganglion cell and outer nuclear layers respectively. Importantly, VEGF-B treatment by intravitreal injection markedly reduced retinal apoptosis in both models. We further reveal that VEGF-B and its receptors, vascular endothelial growth factor 1 (VEGFR1) and neuropilin 1 (NP1), are abundantly expressed in rat retinae and choroids and are upregulated by high glucose with concomitant activation of Akt and Erk. These data highlight an important function of VEGF-B in protecting retinal cells from apoptosis induced by hyperglycemia and VEGF-A inhibition. VEGF-B may therefore have a therapeutic potential in treating various retinal degenerative diseases, and modulation of VEGF-B activity in the eye needs careful consideration. Nature Publishing Group 2016-05-18 /pmc/articles/PMC4870690/ /pubmed/27189805 http://dx.doi.org/10.1038/srep26059 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Article
Huang, Delong
Zhao, Chen
Ju, Rong
Kumar, Anil
Tian, Geng
Huang, Lijuan
Zheng, Lei
Li, Xianglin
Liu, Lixian
Wang, Shasha
Ren, Xiangrong
Ye, Zhimin
Chen, Wei
Xing, Liying
Chen, Qishan
Gao, Zhiqin
Mi, Jia
Tang, Zhongshu
Wang, Bin
Zhang, Shuping
Lee, Chunsik
Li, Xuri
VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title_full VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title_fullStr VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title_full_unstemmed VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title_short VEGF-B inhibits hyperglycemia- and Macugen-induced retinal apoptosis
title_sort vegf-b inhibits hyperglycemia- and macugen-induced retinal apoptosis
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4870690/
https://www.ncbi.nlm.nih.gov/pubmed/27189805
http://dx.doi.org/10.1038/srep26059
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