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Conference Paper: Transgenic mice over-expressing endothelin-1 in endothelial cells have blood-retinal barrier breakdown and lower expression of glial fibrillary acidic protein

TitleTransgenic mice over-expressing endothelin-1 in endothelial cells have blood-retinal barrier breakdown and lower expression of glial fibrillary acidic protein
Authors
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
The Hong Kong Society of Neurosciences 24th Annual Scientific Meeting, Hong Kong, 13-14 January 2005. In Neurosignals, 2006, v. 15 n. 3, p. 121 How to Cite?
AbstractRetinopathy, one of the microvascular complications of diabetes, is a major cause of blindness in adults. The breakdown of blood-retinal barrier (BRB) is a pathogenic feature of diabetic retinopathy (DR). The involvement of endothelin-1 (ET-1) in DR has been suggested by up-regulated ET-1 peptide expression in the retinal endothelial cells of diabetic rats. To investigate the contribution of ET-1 in retinal endothelial cells to morphological, biochemical and functional changes in DR, transgenic mice with endothelial ET-1 over-expression driven by mouse tie-(tyrosine kinase)-1 promoter (TET-1 mice) were generated. Semi-quantitative RT-PCR studies demonstrated that total ET-1 mRNA expression in transgenic mouse retina was increased at least 2-fold. Indeed, immunocytochemical studies showed up-regulation of ET-1 peptide specifically in retinal endothelial cells of TET-1 mice. Moreover, the blood vessel density in the ganglion cell layer of homozygous TET-1 mice was higher than that of non-transgenic mice, indicating that over-expression of ET-1 may lead to neovascularization in retina. On the other hand, the expression of glial fibrillary acidic protein (GFAP) was decreased in optic nerve, astrocytes and Müller cell processes, suggesting that over-expression of ET-1 may down-regulate the expression of GFAP, which is important in the maintenance of BRB. BRB integrity in TET-1 mice was examined by leakage of Evans blue in whole mount retina. Preliminary data showed that there was slightly more focal leakage in retinal blood vessels of TET-1 mice, raising the possibility of ET-1 affecting BRB functions. Our TET-1 mice will be an invaluable model to investigate the contribution of ET-1 in retinal endothelial cells to pathogenic effects of DR.
DescriptionPoster presentation
Persistent Identifierhttp://hdl.handle.net/10722/94958
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763

 

DC FieldValueLanguage
dc.contributor.authorCheung, SFen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorSo, KFen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-25T15:47:13Z-
dc.date.available2010-09-25T15:47:13Z-
dc.date.issued2006en_HK
dc.identifier.citationThe Hong Kong Society of Neurosciences 24th Annual Scientific Meeting, Hong Kong, 13-14 January 2005. In Neurosignals, 2006, v. 15 n. 3, p. 121en_HK
dc.identifier.issn1424-862X-
dc.identifier.urihttp://hdl.handle.net/10722/94958-
dc.descriptionPoster presentation-
dc.description.abstractRetinopathy, one of the microvascular complications of diabetes, is a major cause of blindness in adults. The breakdown of blood-retinal barrier (BRB) is a pathogenic feature of diabetic retinopathy (DR). The involvement of endothelin-1 (ET-1) in DR has been suggested by up-regulated ET-1 peptide expression in the retinal endothelial cells of diabetic rats. To investigate the contribution of ET-1 in retinal endothelial cells to morphological, biochemical and functional changes in DR, transgenic mice with endothelial ET-1 over-expression driven by mouse tie-(tyrosine kinase)-1 promoter (TET-1 mice) were generated. Semi-quantitative RT-PCR studies demonstrated that total ET-1 mRNA expression in transgenic mouse retina was increased at least 2-fold. Indeed, immunocytochemical studies showed up-regulation of ET-1 peptide specifically in retinal endothelial cells of TET-1 mice. Moreover, the blood vessel density in the ganglion cell layer of homozygous TET-1 mice was higher than that of non-transgenic mice, indicating that over-expression of ET-1 may lead to neovascularization in retina. On the other hand, the expression of glial fibrillary acidic protein (GFAP) was decreased in optic nerve, astrocytes and Müller cell processes, suggesting that over-expression of ET-1 may down-regulate the expression of GFAP, which is important in the maintenance of BRB. BRB integrity in TET-1 mice was examined by leakage of Evans blue in whole mount retina. Preliminary data showed that there was slightly more focal leakage in retinal blood vessels of TET-1 mice, raising the possibility of ET-1 affecting BRB functions. Our TET-1 mice will be an invaluable model to investigate the contribution of ET-1 in retinal endothelial cells to pathogenic effects of DR.-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG-
dc.relation.ispartofNeurosignalsen_HK
dc.titleTransgenic mice over-expressing endothelin-1 in endothelial cells have blood-retinal barrier breakdown and lower expression of glial fibrillary acidic proteinen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, SF: simonfai@hkucc.hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailSo, KF: hrmaskf@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authoritySo, KF=rp00329en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000095356-
dc.identifier.hkuros106149en_HK
dc.identifier.spage37en_HK

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