Inflammation and Breakdown of the Blood-Retinal Barrier During "Physiological Aging" in the Rat Retina: A Model for CNS Aging
Objective: To examine the possible contribution of inflammation and breakdown of the blood-brain barrier in the central nervous system (CNS) of physiologically aged rats showing cognitive decline. Methods: Young (3- to 6-month-old) and aged (24- to 30-month-old) Wistar rats were assessed by the nove...
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Veröffentlicht in: | Microcirculation (New York, N.Y. 1994) N.Y. 1994), 2007, Vol.14 (1), p.63-76 |
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creator | Chan-Ling, Tailoi Hughes, Suzanne Baxter, Louise Rosinova, Emelia McGregor, Iain Morcos, Yvette van Nieuwenhuyzen, Petra Hu, Ping |
description | Objective: To examine the possible contribution of inflammation and breakdown of the blood-brain barrier in the central nervous system (CNS) of physiologically aged rats showing cognitive decline.
Methods: Young (3- to 6-month-old) and aged (24- to 30-month-old) Wistar rats were assessed by the novel object recognition test. Vascular and inflammatory changes in the CNS were investigated in whole-mount preparations or sections of retinas from young adult or aged male Wistar rats.
Results: Aged rats showed a significant impairment in short-term memory compared with young adults. Deterioration of blood-retinal barrier function in aged rats was evidenced by leakage of intravascular tracer into the retinal parenchyma and reduced immunoreactivity for the tight junctional protein, occludin. Immunohistochemistry revealed the presence of major histocompatibility complex (MHC) class II-positive resident microglia, activated T cells, and monocyte-like cells in the retinal parenchyma of aged rats only. Microglia positive for the ED1 antigen, indicative of phagocytic activity, were also observed in these retinas.
Conclusion: Breakdown of the blood-retinal barrier, MHC class II expression, microglial activation, and trafficking of activated T cells are associated with physiological aging. Such changes in the CNS may contribute to the pathogenesis of age-related cognitive decline. |
doi_str_mv | 10.1080/10739680601073451 |
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Methods: Young (3- to 6-month-old) and aged (24- to 30-month-old) Wistar rats were assessed by the novel object recognition test. Vascular and inflammatory changes in the CNS were investigated in whole-mount preparations or sections of retinas from young adult or aged male Wistar rats.
Results: Aged rats showed a significant impairment in short-term memory compared with young adults. Deterioration of blood-retinal barrier function in aged rats was evidenced by leakage of intravascular tracer into the retinal parenchyma and reduced immunoreactivity for the tight junctional protein, occludin. Immunohistochemistry revealed the presence of major histocompatibility complex (MHC) class II-positive resident microglia, activated T cells, and monocyte-like cells in the retinal parenchyma of aged rats only. Microglia positive for the ED1 antigen, indicative of phagocytic activity, were also observed in these retinas.
Conclusion: Breakdown of the blood-retinal barrier, MHC class II expression, microglial activation, and trafficking of activated T cells are associated with physiological aging. Such changes in the CNS may contribute to the pathogenesis of age-related cognitive decline.</description><identifier>ISSN: 1073-9688</identifier><identifier>EISSN: 1549-8719</identifier><identifier>DOI: 10.1080/10739680601073451</identifier><identifier>PMID: 17365662</identifier><language>eng</language><publisher>Oxford, UK: Informa UK Ltd</publisher><subject>Aging - immunology ; Aging - pathology ; Animals ; Antibodies ; antigen presentation ; blood-brain barrier ; Blood-Brain Barrier - immunology ; Blood-Brain Barrier - pathology ; blood-retinal barrier ; Cognition Disorders - immunology ; Cognition Disorders - pathology ; Disease Models, Animal ; Ectodysplasins - metabolism ; Female ; Histocompatibility Antigens Class II - metabolism ; Horseradish Peroxidase ; Indicators and Reagents ; Indoles ; inflammation ; Inflammation - immunology ; Inflammation - pathology ; Inflammation - physiopathology ; Male ; Membrane Proteins - immunology ; Microcirculation - immunology ; microglia ; Microglia - immunology ; Microglia - metabolism ; Microglia - pathology ; Monocytes - immunology ; Monocytes - metabolism ; Monocytes - pathology ; neurodegeneration ; Occludin ; Organometallic Compounds ; Protein Transport - immunology ; Rats ; Rats, Wistar ; retina ; Retinal Vessels - immunology ; Retinal Vessels - pathology ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology ; Tight Junctions - physiology</subject><ispartof>Microcirculation (New York, N.Y. 1994), 2007, Vol.14 (1), p.63-76</ispartof><rights>2007 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2007</rights><rights>2007 Blackwell</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4790-245aa928becc45c7f4371943b9740b469c3f361eb121edb6ad45ba7fbf81ab5a3</citedby><cites>FETCH-LOGICAL-c4790-245aa928becc45c7f4371943b9740b469c3f361eb121edb6ad45ba7fbf81ab5a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/10739680601073451$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/10739680601073451$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>314,780,784,1417,4023,27922,27923,27924,45573,45574,61220,61401</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17365662$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chan-Ling, Tailoi</creatorcontrib><creatorcontrib>Hughes, Suzanne</creatorcontrib><creatorcontrib>Baxter, Louise</creatorcontrib><creatorcontrib>Rosinova, Emelia</creatorcontrib><creatorcontrib>McGregor, Iain</creatorcontrib><creatorcontrib>Morcos, Yvette</creatorcontrib><creatorcontrib>van Nieuwenhuyzen, Petra</creatorcontrib><creatorcontrib>Hu, Ping</creatorcontrib><title>Inflammation and Breakdown of the Blood-Retinal Barrier During "Physiological Aging" in the Rat Retina: A Model for CNS Aging</title><title>Microcirculation (New York, N.Y. 1994)</title><addtitle>Microcirculation</addtitle><description>Objective: To examine the possible contribution of inflammation and breakdown of the blood-brain barrier in the central nervous system (CNS) of physiologically aged rats showing cognitive decline.
Methods: Young (3- to 6-month-old) and aged (24- to 30-month-old) Wistar rats were assessed by the novel object recognition test. Vascular and inflammatory changes in the CNS were investigated in whole-mount preparations or sections of retinas from young adult or aged male Wistar rats.
Results: Aged rats showed a significant impairment in short-term memory compared with young adults. Deterioration of blood-retinal barrier function in aged rats was evidenced by leakage of intravascular tracer into the retinal parenchyma and reduced immunoreactivity for the tight junctional protein, occludin. Immunohistochemistry revealed the presence of major histocompatibility complex (MHC) class II-positive resident microglia, activated T cells, and monocyte-like cells in the retinal parenchyma of aged rats only. Microglia positive for the ED1 antigen, indicative of phagocytic activity, were also observed in these retinas.
Conclusion: Breakdown of the blood-retinal barrier, MHC class II expression, microglial activation, and trafficking of activated T cells are associated with physiological aging. Such changes in the CNS may contribute to the pathogenesis of age-related cognitive decline.</description><subject>Aging - immunology</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>antigen presentation</subject><subject>blood-brain barrier</subject><subject>Blood-Brain Barrier - immunology</subject><subject>Blood-Brain Barrier - pathology</subject><subject>blood-retinal barrier</subject><subject>Cognition Disorders - immunology</subject><subject>Cognition Disorders - pathology</subject><subject>Disease Models, Animal</subject><subject>Ectodysplasins - metabolism</subject><subject>Female</subject><subject>Histocompatibility Antigens Class II - metabolism</subject><subject>Horseradish Peroxidase</subject><subject>Indicators and Reagents</subject><subject>Indoles</subject><subject>inflammation</subject><subject>Inflammation - immunology</subject><subject>Inflammation - pathology</subject><subject>Inflammation - physiopathology</subject><subject>Male</subject><subject>Membrane Proteins - immunology</subject><subject>Microcirculation - immunology</subject><subject>microglia</subject><subject>Microglia - immunology</subject><subject>Microglia - metabolism</subject><subject>Microglia - pathology</subject><subject>Monocytes - immunology</subject><subject>Monocytes - metabolism</subject><subject>Monocytes - pathology</subject><subject>neurodegeneration</subject><subject>Occludin</subject><subject>Organometallic Compounds</subject><subject>Protein Transport - immunology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>retina</subject><subject>Retinal Vessels - immunology</subject><subject>Retinal Vessels - pathology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><subject>Tight Junctions - physiology</subject><issn>1073-9688</issn><issn>1549-8719</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhiNERUvhB3BBVg-9hdqJPxI47QbaLtouqHwdrYnj7Lp14mInKnvgv-NtVnBAgpNH4-cZeV4nyQuCXxFc4DOCRV7yAnO8qygjj5IjwmiZFoKUj2Mdu2kEisPkaQg3GOOiyMonySEROWecZ0fJz0XfWug6GIzrEfQNmnsNt42775Fr0bDRaG6da9JrPZgeLJqD90Z79Hb0pl-jk4-bbTDOurVR8Xa2js0TZPoH8xoGNHmv0QxduUZb1DqPqtWniXyWHLRgg36-P4-TL-fvPleX6fLDxaKaLVNFRYnTjDKAMitqrRRlSrQ0jwvSvC4FxTXlpcrbnBNdk4zopubQUFaDaOu2IFAzyI-T02nunXffRx0G2ZmgtLXQazcGKXAmOCtFBMkEKu9C8LqVd9504LeSYLnLXP6VeXRe7oePdaebP8Y-5AjwCbg3Vm__P1FeLaqKcRzFdBJNGPSP3yL4W8lFLpj8trqQdPWVndP3S7l7yZs938eYO9hosMNGgdfyxo0-fl_4xx6_ABh0rCw</recordid><startdate>2007</startdate><enddate>2007</enddate><creator>Chan-Ling, Tailoi</creator><creator>Hughes, Suzanne</creator><creator>Baxter, Louise</creator><creator>Rosinova, Emelia</creator><creator>McGregor, Iain</creator><creator>Morcos, Yvette</creator><creator>van Nieuwenhuyzen, Petra</creator><creator>Hu, Ping</creator><general>Informa UK Ltd</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>2007</creationdate><title>Inflammation and Breakdown of the Blood-Retinal Barrier During "Physiological Aging" in the Rat Retina: A Model for CNS Aging</title><author>Chan-Ling, Tailoi ; Hughes, Suzanne ; Baxter, Louise ; Rosinova, Emelia ; McGregor, Iain ; Morcos, Yvette ; van Nieuwenhuyzen, Petra ; Hu, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4790-245aa928becc45c7f4371943b9740b469c3f361eb121edb6ad45ba7fbf81ab5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Aging - immunology</topic><topic>Aging - pathology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>antigen presentation</topic><topic>blood-brain barrier</topic><topic>Blood-Brain Barrier - immunology</topic><topic>Blood-Brain Barrier - pathology</topic><topic>blood-retinal barrier</topic><topic>Cognition Disorders - immunology</topic><topic>Cognition Disorders - pathology</topic><topic>Disease Models, Animal</topic><topic>Ectodysplasins - metabolism</topic><topic>Female</topic><topic>Histocompatibility Antigens Class II - metabolism</topic><topic>Horseradish Peroxidase</topic><topic>Indicators and Reagents</topic><topic>Indoles</topic><topic>inflammation</topic><topic>Inflammation - immunology</topic><topic>Inflammation - pathology</topic><topic>Inflammation - physiopathology</topic><topic>Male</topic><topic>Membrane Proteins - immunology</topic><topic>Microcirculation - immunology</topic><topic>microglia</topic><topic>Microglia - immunology</topic><topic>Microglia - metabolism</topic><topic>Microglia - pathology</topic><topic>Monocytes - immunology</topic><topic>Monocytes - metabolism</topic><topic>Monocytes - pathology</topic><topic>neurodegeneration</topic><topic>Occludin</topic><topic>Organometallic Compounds</topic><topic>Protein Transport - immunology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>retina</topic><topic>Retinal Vessels - immunology</topic><topic>Retinal Vessels - pathology</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><topic>Tight Junctions - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chan-Ling, Tailoi</creatorcontrib><creatorcontrib>Hughes, Suzanne</creatorcontrib><creatorcontrib>Baxter, Louise</creatorcontrib><creatorcontrib>Rosinova, Emelia</creatorcontrib><creatorcontrib>McGregor, Iain</creatorcontrib><creatorcontrib>Morcos, Yvette</creatorcontrib><creatorcontrib>van Nieuwenhuyzen, Petra</creatorcontrib><creatorcontrib>Hu, Ping</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Microcirculation (New York, N.Y. 1994)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chan-Ling, Tailoi</au><au>Hughes, Suzanne</au><au>Baxter, Louise</au><au>Rosinova, Emelia</au><au>McGregor, Iain</au><au>Morcos, Yvette</au><au>van Nieuwenhuyzen, Petra</au><au>Hu, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inflammation and Breakdown of the Blood-Retinal Barrier During "Physiological Aging" in the Rat Retina: A Model for CNS Aging</atitle><jtitle>Microcirculation (New York, N.Y. 1994)</jtitle><addtitle>Microcirculation</addtitle><date>2007</date><risdate>2007</risdate><volume>14</volume><issue>1</issue><spage>63</spage><epage>76</epage><pages>63-76</pages><issn>1073-9688</issn><eissn>1549-8719</eissn><abstract>Objective: To examine the possible contribution of inflammation and breakdown of the blood-brain barrier in the central nervous system (CNS) of physiologically aged rats showing cognitive decline.
Methods: Young (3- to 6-month-old) and aged (24- to 30-month-old) Wistar rats were assessed by the novel object recognition test. Vascular and inflammatory changes in the CNS were investigated in whole-mount preparations or sections of retinas from young adult or aged male Wistar rats.
Results: Aged rats showed a significant impairment in short-term memory compared with young adults. Deterioration of blood-retinal barrier function in aged rats was evidenced by leakage of intravascular tracer into the retinal parenchyma and reduced immunoreactivity for the tight junctional protein, occludin. Immunohistochemistry revealed the presence of major histocompatibility complex (MHC) class II-positive resident microglia, activated T cells, and monocyte-like cells in the retinal parenchyma of aged rats only. Microglia positive for the ED1 antigen, indicative of phagocytic activity, were also observed in these retinas.
Conclusion: Breakdown of the blood-retinal barrier, MHC class II expression, microglial activation, and trafficking of activated T cells are associated with physiological aging. Such changes in the CNS may contribute to the pathogenesis of age-related cognitive decline.</abstract><cop>Oxford, UK</cop><pub>Informa UK Ltd</pub><pmid>17365662</pmid><doi>10.1080/10739680601073451</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aging - immunology Aging - pathology Animals Antibodies antigen presentation blood-brain barrier Blood-Brain Barrier - immunology Blood-Brain Barrier - pathology blood-retinal barrier Cognition Disorders - immunology Cognition Disorders - pathology Disease Models, Animal Ectodysplasins - metabolism Female Histocompatibility Antigens Class II - metabolism Horseradish Peroxidase Indicators and Reagents Indoles inflammation Inflammation - immunology Inflammation - pathology Inflammation - physiopathology Male Membrane Proteins - immunology Microcirculation - immunology microglia Microglia - immunology Microglia - metabolism Microglia - pathology Monocytes - immunology Monocytes - metabolism Monocytes - pathology neurodegeneration Occludin Organometallic Compounds Protein Transport - immunology Rats Rats, Wistar retina Retinal Vessels - immunology Retinal Vessels - pathology T-Lymphocytes - immunology T-Lymphocytes - pathology Tight Junctions - physiology |
title | Inflammation and Breakdown of the Blood-Retinal Barrier During "Physiological Aging" in the Rat Retina: A Model for CNS Aging |
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