Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells.
Vascular endothelial growth factor (VEGF) is a major regulator in retinal and choroidal angiogenesis, which are common causes of blindness in all age groups. Recently anti-VEGF treatment using anti-VEGF antibody has revolutionarily improved the visual outcome in patients with vaso-proliferative reti...
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doaj-acadc0ee6a57457bb839df489fbaf7692020-11-25T01:46:18ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0173e3345610.1371/journal.pone.0033456Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells.Jang Won HeoJin Hyoung KimChang Sik ChoHyoung Oh JunDong Hun KimYoung Suk YuJeong Hun KimVascular endothelial growth factor (VEGF) is a major regulator in retinal and choroidal angiogenesis, which are common causes of blindness in all age groups. Recently anti-VEGF treatment using anti-VEGF antibody has revolutionarily improved the visual outcome in patients with vaso-proliferative retinopathies. Herein, we demonstrated that bevacizumab as an anti-VEGF antibody could inhibit differentiation of retinoblastoma cells without affection to cellular viability, which would be mediated via blockade of extracellular signal-regulated kinase (ERK) 1/2 activation. The retinoblastoma cells expressed VEGFR-2 as well as TrkA which is a neurotrophin receptor associated with differentiation of retinoblastoma cells. TrkA in retinoblastoma cells was activated with VEGF treatment. Interestingly even in the concentration of no cellular death, bevascizumab significantly attenuated the neurite formation of differentiated retinoblastoma cells, which was accompanied by inhibition of neurofilament and shank2 expression. Furthermore, bevacizumab inhibited differentiation of retinoblastoma cells by blockade of ERK 1/2 activation. Therefore, based on that the differentiated retinoblastoma cells are mostly photoreceptors, our results suggest that anti-VEGF therapies would affect to the maintenance or function of photoreceptors in mature retina.http://europepmc.org/articles/PMC3310877?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Jang Won Heo Jin Hyoung Kim Chang Sik Cho Hyoung Oh Jun Dong Hun Kim Young Suk Yu Jeong Hun Kim |
spellingShingle |
Jang Won Heo Jin Hyoung Kim Chang Sik Cho Hyoung Oh Jun Dong Hun Kim Young Suk Yu Jeong Hun Kim Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. PLoS ONE |
author_facet |
Jang Won Heo Jin Hyoung Kim Chang Sik Cho Hyoung Oh Jun Dong Hun Kim Young Suk Yu Jeong Hun Kim |
author_sort |
Jang Won Heo |
title |
Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
title_short |
Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
title_full |
Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
title_fullStr |
Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
title_full_unstemmed |
Inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
title_sort |
inhibitory activity of bevacizumab to differentiation of retinoblastoma cells. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2012-01-01 |
description |
Vascular endothelial growth factor (VEGF) is a major regulator in retinal and choroidal angiogenesis, which are common causes of blindness in all age groups. Recently anti-VEGF treatment using anti-VEGF antibody has revolutionarily improved the visual outcome in patients with vaso-proliferative retinopathies. Herein, we demonstrated that bevacizumab as an anti-VEGF antibody could inhibit differentiation of retinoblastoma cells without affection to cellular viability, which would be mediated via blockade of extracellular signal-regulated kinase (ERK) 1/2 activation. The retinoblastoma cells expressed VEGFR-2 as well as TrkA which is a neurotrophin receptor associated with differentiation of retinoblastoma cells. TrkA in retinoblastoma cells was activated with VEGF treatment. Interestingly even in the concentration of no cellular death, bevascizumab significantly attenuated the neurite formation of differentiated retinoblastoma cells, which was accompanied by inhibition of neurofilament and shank2 expression. Furthermore, bevacizumab inhibited differentiation of retinoblastoma cells by blockade of ERK 1/2 activation. Therefore, based on that the differentiated retinoblastoma cells are mostly photoreceptors, our results suggest that anti-VEGF therapies would affect to the maintenance or function of photoreceptors in mature retina. |
url |
http://europepmc.org/articles/PMC3310877?pdf=render |
work_keys_str_mv |
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