Changes in components of the neurovascular unit in the retina in a rat model of retinopathy of prematurity
An impairment of cellular interactions between the elements of the neurovascular unit contributes to the onset and/or progression of retinal diseases. The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rat...
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| Veröffentlicht in: | Cell and tissue research 2020-03, Vol.379 (3), p.473-486 |
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| creator | Nakano, Ayuki Kondo, Ryo Kaneko, Yuki Arima, Shiho Asano, Daiki Morita, Akane Sakamoto, Kenji Nagamitsu, Tohru Nakahara, Tsutomu |
| description | An impairment of cellular interactions between the elements of the neurovascular unit contributes to the onset and/or progression of retinal diseases. The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP. Morphological assessments were performed of blood vessels, astrocytes and neuronal cells in the retina. Aggressive angiogenesis, tortuous arteries and enlarged veins were observed in the retinal vasculature of KRN633-treated (ROP) rats from P14 to P28, compared to age-matched control (vehicle-treated) animals. Morphological abnormalities in the retinal vasculature showed a tendency toward spontaneous recovery from P28 to P35 in ROP rats. Immunofluorescence staining for glial fibrillary acidic protein and Pax2 (astrocyte markers) revealed that morphological changes to and a reduction in the number of astrocytes occurred in ROP rats. The developmental cell death was slightly accelerated in ROP rats; however, no visible changes in the morphology of retinal layers were observed on P35. The abnormalities in astrocytes might contribute, at least in part, to the formation of abnormal retinal blood vessels and the pathogenesis of ROP. |
| doi_str_mv | 10.1007/s00441-019-03112-9 |
| format | Article |
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The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP. Morphological assessments were performed of blood vessels, astrocytes and neuronal cells in the retina. Aggressive angiogenesis, tortuous arteries and enlarged veins were observed in the retinal vasculature of KRN633-treated (ROP) rats from P14 to P28, compared to age-matched control (vehicle-treated) animals. Morphological abnormalities in the retinal vasculature showed a tendency toward spontaneous recovery from P28 to P35 in ROP rats. Immunofluorescence staining for glial fibrillary acidic protein and Pax2 (astrocyte markers) revealed that morphological changes to and a reduction in the number of astrocytes occurred in ROP rats. The developmental cell death was slightly accelerated in ROP rats; however, no visible changes in the morphology of retinal layers were observed on P35. The abnormalities in astrocytes might contribute, at least in part, to the formation of abnormal retinal blood vessels and the pathogenesis of ROP.</description><identifier>ISSN: 0302-766X</identifier><identifier>EISSN: 1432-0878</identifier><identifier>DOI: 10.1007/s00441-019-03112-9</identifier><identifier>PMID: 31788758</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Angiogenesis ; Arteries ; Astrocytes ; Biomedical and Life Sciences ; Biomedicine ; Blood vessels ; Cell death ; Enzyme inhibitors ; Glial fibrillary acidic protein ; Human Genetics ; Immunofluorescence ; Molecular Medicine ; Morphology ; Neonates ; Pax2 protein ; Protein-tyrosine kinase receptors ; Proteomics ; Regular Article ; Retina ; Retinopathy ; Retrolental fibroplasia ; Spontaneous recovery ; Vascular endothelial growth factor</subject><ispartof>Cell and tissue research, 2020-03, Vol.379 (3), p.473-486</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>COPYRIGHT 2020 Springer</rights><rights>Cell and Tissue Research is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c539t-1cafbd928db408562611499be3b253048a434cd94322d612b4860d2ac15d7c7a3</citedby><cites>FETCH-LOGICAL-c539t-1cafbd928db408562611499be3b253048a434cd94322d612b4860d2ac15d7c7a3</cites><orcidid>0000-0001-7579-5870</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00441-019-03112-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00441-019-03112-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31788758$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakano, Ayuki</creatorcontrib><creatorcontrib>Kondo, Ryo</creatorcontrib><creatorcontrib>Kaneko, Yuki</creatorcontrib><creatorcontrib>Arima, Shiho</creatorcontrib><creatorcontrib>Asano, Daiki</creatorcontrib><creatorcontrib>Morita, Akane</creatorcontrib><creatorcontrib>Sakamoto, Kenji</creatorcontrib><creatorcontrib>Nagamitsu, Tohru</creatorcontrib><creatorcontrib>Nakahara, Tsutomu</creatorcontrib><title>Changes in components of the neurovascular unit in the retina in a rat model of retinopathy of prematurity</title><title>Cell and tissue research</title><addtitle>Cell Tissue Res</addtitle><addtitle>Cell Tissue Res</addtitle><description>An impairment of cellular interactions between the elements of the neurovascular unit contributes to the onset and/or progression of retinal diseases. The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP. Morphological assessments were performed of blood vessels, astrocytes and neuronal cells in the retina. Aggressive angiogenesis, tortuous arteries and enlarged veins were observed in the retinal vasculature of KRN633-treated (ROP) rats from P14 to P28, compared to age-matched control (vehicle-treated) animals. Morphological abnormalities in the retinal vasculature showed a tendency toward spontaneous recovery from P28 to P35 in ROP rats. Immunofluorescence staining for glial fibrillary acidic protein and Pax2 (astrocyte markers) revealed that morphological changes to and a reduction in the number of astrocytes occurred in ROP rats. The developmental cell death was slightly accelerated in ROP rats; however, no visible changes in the morphology of retinal layers were observed on P35. The abnormalities in astrocytes might contribute, at least in part, to the formation of abnormal retinal blood vessels and the pathogenesis of ROP.</description><subject>Angiogenesis</subject><subject>Arteries</subject><subject>Astrocytes</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood vessels</subject><subject>Cell death</subject><subject>Enzyme inhibitors</subject><subject>Glial fibrillary acidic protein</subject><subject>Human Genetics</subject><subject>Immunofluorescence</subject><subject>Molecular Medicine</subject><subject>Morphology</subject><subject>Neonates</subject><subject>Pax2 protein</subject><subject>Protein-tyrosine kinase receptors</subject><subject>Proteomics</subject><subject>Regular Article</subject><subject>Retina</subject><subject>Retinopathy</subject><subject>Retrolental fibroplasia</subject><subject>Spontaneous recovery</subject><subject>Vascular endothelial growth 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Res</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>379</volume><issue>3</issue><spage>473</spage><epage>486</epage><pages>473-486</pages><issn>0302-766X</issn><eissn>1432-0878</eissn><abstract>An impairment of cellular interactions between the elements of the neurovascular unit contributes to the onset and/or progression of retinal diseases. The present study aims to examine how elements of the neurovascular unit are altered in a rat model of retinopathy of prematurity (ROP). Neonatal rats were treated subcutaneously with the vascular endothelial growth factor (VEGF) receptor tyrosine kinase inhibitor KRN633 (10 mg/kg) on postnatal day (P) 7 and P8 to induce ROP. Morphological assessments were performed of blood vessels, astrocytes and neuronal cells in the retina. Aggressive angiogenesis, tortuous arteries and enlarged veins were observed in the retinal vasculature of KRN633-treated (ROP) rats from P14 to P28, compared to age-matched control (vehicle-treated) animals. Morphological abnormalities in the retinal vasculature showed a tendency toward spontaneous recovery from P28 to P35 in ROP rats. Immunofluorescence staining for glial fibrillary acidic protein and Pax2 (astrocyte markers) revealed that morphological changes to and a reduction in the number of astrocytes occurred in ROP rats. The developmental cell death was slightly accelerated in ROP rats; however, no visible changes in the morphology of retinal layers were observed on P35. The abnormalities in astrocytes might contribute, at least in part, to the formation of abnormal retinal blood vessels and the pathogenesis of ROP.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31788758</pmid><doi>10.1007/s00441-019-03112-9</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7579-5870</orcidid></addata></record> |
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| subjects | Angiogenesis Arteries Astrocytes Biomedical and Life Sciences Biomedicine Blood vessels Cell death Enzyme inhibitors Glial fibrillary acidic protein Human Genetics Immunofluorescence Molecular Medicine Morphology Neonates Pax2 protein Protein-tyrosine kinase receptors Proteomics Regular Article Retina Retinopathy Retrolental fibroplasia Spontaneous recovery Vascular endothelial growth factor |
| title | Changes in components of the neurovascular unit in the retina in a rat model of retinopathy of prematurity |
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