Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat
Peter JB Anderson1,a, HR Watts1,a, CJ Hille3, KL Philpott3, P Clark4, M Croucher, S Gentleman2, Ling-Sun Jen11Department of Cellular and Molecular Neuroscience; 2Department of Clinical Neuroscience, Division of Neuroscience and Mental Health, Imperial College London, Charing Cross Hospital Campus, L...
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Dove Medical Press
2008
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oai:doaj.org-article:f9123dbfaa3242009c31e7f5c0b885992021-12-02T06:17:08ZGlial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat1177-54671177-5483https://doaj.org/article/f9123dbfaa3242009c31e7f5c0b885992008-11-01T00:00:00Zhttp://www.dovepress.com/glial-and-endothelial-blood-retinal-barrier-responses-to-amyloid-beta--a2563https://doaj.org/toc/1177-5467https://doaj.org/toc/1177-5483Peter JB Anderson1,a, HR Watts1,a, CJ Hille3, KL Philpott3, P Clark4, M Croucher, S Gentleman2, Ling-Sun Jen11Department of Cellular and Molecular Neuroscience; 2Department of Clinical Neuroscience, Division of Neuroscience and Mental Health, Imperial College London, Charing Cross Hospital Campus, London, UK; 3Neurosciences, Centre of Excellence for Drug Discovery, GlaxoSmithKline Pharmaceuticals, Harlow, Essex, UK; 4Leukocyte Biology Section, National Heart and Lung Institute, Imperial College London, London, UK; aThese researchers contributed equally to this paperAbstract: The effects of an intravitreal or subretinal injection of soluble or aggregated forms of Aβ1–42 on retinal nestin-immunoreactivity (-IR) and glial fibrillary acidic protein (GFAP)-IR in astrocytes and Müller glial cells and the integrity of the blood-retinal barrier (BRB) were tested in the in vivo rat vitreal-retinal model. Retinas were exposed for 1, 2, 3, 5 or 30 days. We present novel data demonstrating that aggregated Aβ1–42 up-regulates nestin-IR in astrocytes and Müller cells, with a graded response directly related to the length of pre-injection aggregation time. Similar results were obtained with GFAP-IR, but the signal was weaker. An intravitreal injection of aggregated Aβ1–42 led to VEGF-IR up-regulation, particularly in the GCL and to a lesser extent in the INL. VEGFR1-IR (Flt1) was also increased, particularly in Müller cells and this was accompanied by marked leakage of albumin into the retinal parenchyma of the injected eye, but not in the contralateral eye.Keywords: amyloid-β, Müller cells, blood-retinal barrier Peter JB AndersonHR WattsCJ HilleKL PhilpottP Clarket alDove Medical PressarticleOphthalmologyRE1-994ENClinical Ophthalmology, Vol 2008, Iss Issue 4, Pp 801-816 (2008) |
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Ophthalmology RE1-994 Peter JB Anderson HR Watts CJ Hille KL Philpott P Clark et al Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
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Peter JB Anderson1,a, HR Watts1,a, CJ Hille3, KL Philpott3, P Clark4, M Croucher, S Gentleman2, Ling-Sun Jen11Department of Cellular and Molecular Neuroscience; 2Department of Clinical Neuroscience, Division of Neuroscience and Mental Health, Imperial College London, Charing Cross Hospital Campus, London, UK; 3Neurosciences, Centre of Excellence for Drug Discovery, GlaxoSmithKline Pharmaceuticals, Harlow, Essex, UK; 4Leukocyte Biology Section, National Heart and Lung Institute, Imperial College London, London, UK; aThese researchers contributed equally to this paperAbstract: The effects of an intravitreal or subretinal injection of soluble or aggregated forms of Aβ1–42 on retinal nestin-immunoreactivity (-IR) and glial fibrillary acidic protein (GFAP)-IR in astrocytes and Müller glial cells and the integrity of the blood-retinal barrier (BRB) were tested in the in vivo rat vitreal-retinal model. Retinas were exposed for 1, 2, 3, 5 or 30 days. We present novel data demonstrating that aggregated Aβ1–42 up-regulates nestin-IR in astrocytes and Müller cells, with a graded response directly related to the length of pre-injection aggregation time. Similar results were obtained with GFAP-IR, but the signal was weaker. An intravitreal injection of aggregated Aβ1–42 led to VEGF-IR up-regulation, particularly in the GCL and to a lesser extent in the INL. VEGFR1-IR (Flt1) was also increased, particularly in Müller cells and this was accompanied by marked leakage of albumin into the retinal parenchyma of the injected eye, but not in the contralateral eye.Keywords: amyloid-β, Müller cells, blood-retinal barrier |
format |
article |
author |
Peter JB Anderson HR Watts CJ Hille KL Philpott P Clark et al |
author_facet |
Peter JB Anderson HR Watts CJ Hille KL Philpott P Clark et al |
author_sort |
Peter JB Anderson |
title |
Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
title_short |
Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
title_full |
Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
title_fullStr |
Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
title_full_unstemmed |
Glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
title_sort |
glial and endothelial blood-retinal barrier responses to amyloid-β in the neural retina of the rat |
publisher |
Dove Medical Press |
publishDate |
2008 |
url |
https://doaj.org/article/f9123dbfaa3242009c31e7f5c0b88599 |
work_keys_str_mv |
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