Expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis
The expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE) was analyzed. Western blot analysis showed that three isotypes of caveolins including caveolin-1, -2 and -3 increased significantly in the spinal cords of rats during the e...
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| Veröffentlicht in: | Journal of neuroimmunology 2005-08, Vol.165 (1), p.11-20 |
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| creator | Shin, Taekyun Kim, Heechul Jin, Jae-kwang Moon, Changjong Ahn, Meejung Tanuma, Naoyuki Matsumoto, Yoh |
| description | The expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE) was analyzed. Western blot analysis showed that three isotypes of caveolins including caveolin-1, -2 and -3 increased significantly in the spinal cords of rats during the early stage of EAE, as compared with the levels in control animals (
p
<
0.05); the elevated level of each caveolin persisted during the peak and recovery stage of EAE. Immunohistochemistry demonstrated that caveolin-1 and -2 were expressed constitutively in the vascular endothelial cells and ependymal cells of the normal rat spinal cord, whereas caveolin-3 was almost exclusively localized in astrocytes. In EAE lesions, the immunoreactivity of caveolin-1 was increased in the ependymal cells, some astrocytes, and some inflammatory cells of the spinal cord, while that of caveolin-2 showed an intense immunoreactivity. Caveolin-3 was expressed constitutively in some astrocytes, but not in endothelial cells; its immunoreactivity was increased in reactive astrocytes in EAE lesions. The results of the Western blot analysis largely confirmed the observations obtained with immunohistochemistry.
Taking all the findings into consideration, we postulate that the expression levels of each caveolin begin to increase when EAE is initiated, possibly contributing to the modulation of signal transduction pathways in the affected cells. |
| doi_str_mv | 10.1016/j.jneuroim.2005.03.019 |
| format | Article |
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p
<
0.05); the elevated level of each caveolin persisted during the peak and recovery stage of EAE. Immunohistochemistry demonstrated that caveolin-1 and -2 were expressed constitutively in the vascular endothelial cells and ependymal cells of the normal rat spinal cord, whereas caveolin-3 was almost exclusively localized in astrocytes. In EAE lesions, the immunoreactivity of caveolin-1 was increased in the ependymal cells, some astrocytes, and some inflammatory cells of the spinal cord, while that of caveolin-2 showed an intense immunoreactivity. Caveolin-3 was expressed constitutively in some astrocytes, but not in endothelial cells; its immunoreactivity was increased in reactive astrocytes in EAE lesions. The results of the Western blot analysis largely confirmed the observations obtained with immunohistochemistry.
Taking all the findings into consideration, we postulate that the expression levels of each caveolin begin to increase when EAE is initiated, possibly contributing to the modulation of signal transduction pathways in the affected cells.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/j.jneuroim.2005.03.019</identifier><identifier>PMID: 15925413</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Astrocyte ; Caveolin ; Caveolin 1 ; Caveolin 2 ; Caveolin 3 ; Caveolins - biosynthesis ; Caveolins - immunology ; Caveolins - metabolism ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Experimental autoimmune encephalomyelitis ; Female ; Immune Sera ; Immunohistochemistry ; Immunophenotyping ; Microglia/macrophage ; Neuroglia - immunology ; Neuroglia - metabolism ; Neuroglia - pathology ; Neurons - chemistry ; Neurons - metabolism ; Neurons - pathology ; Protein Isoforms - biosynthesis ; Protein Isoforms - immunology ; Protein Isoforms - metabolism ; Rats ; Rats, Inbred Lew ; Receptors, Antigen, T-Cell, alpha-beta - biosynthesis ; Spinal Cord - metabolism ; Spinal Cord - pathology ; Up-Regulation</subject><ispartof>Journal of neuroimmunology, 2005-08, Vol.165 (1), p.11-20</ispartof><rights>2005 Elsevier B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c397t-f23ed02e7f2e0611e4f3a263aaabb3c670b1b33d88547a0e6a790dfdf58dc893</citedby><cites>FETCH-LOGICAL-c397t-f23ed02e7f2e0611e4f3a263aaabb3c670b1b33d88547a0e6a790dfdf58dc893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0165572805001244$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15925413$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Taekyun</creatorcontrib><creatorcontrib>Kim, Heechul</creatorcontrib><creatorcontrib>Jin, Jae-kwang</creatorcontrib><creatorcontrib>Moon, Changjong</creatorcontrib><creatorcontrib>Ahn, Meejung</creatorcontrib><creatorcontrib>Tanuma, Naoyuki</creatorcontrib><creatorcontrib>Matsumoto, Yoh</creatorcontrib><title>Expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>The expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE) was analyzed. Western blot analysis showed that three isotypes of caveolins including caveolin-1, -2 and -3 increased significantly in the spinal cords of rats during the early stage of EAE, as compared with the levels in control animals (
p
<
0.05); the elevated level of each caveolin persisted during the peak and recovery stage of EAE. Immunohistochemistry demonstrated that caveolin-1 and -2 were expressed constitutively in the vascular endothelial cells and ependymal cells of the normal rat spinal cord, whereas caveolin-3 was almost exclusively localized in astrocytes. In EAE lesions, the immunoreactivity of caveolin-1 was increased in the ependymal cells, some astrocytes, and some inflammatory cells of the spinal cord, while that of caveolin-2 showed an intense immunoreactivity. Caveolin-3 was expressed constitutively in some astrocytes, but not in endothelial cells; its immunoreactivity was increased in reactive astrocytes in EAE lesions. The results of the Western blot analysis largely confirmed the observations obtained with immunohistochemistry.
Taking all the findings into consideration, we postulate that the expression levels of each caveolin begin to increase when EAE is initiated, possibly contributing to the modulation of signal transduction pathways in the affected cells.</description><subject>Animals</subject><subject>Astrocyte</subject><subject>Caveolin</subject><subject>Caveolin 1</subject><subject>Caveolin 2</subject><subject>Caveolin 3</subject><subject>Caveolins - biosynthesis</subject><subject>Caveolins - immunology</subject><subject>Caveolins - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Experimental autoimmune encephalomyelitis</subject><subject>Female</subject><subject>Immune Sera</subject><subject>Immunohistochemistry</subject><subject>Immunophenotyping</subject><subject>Microglia/macrophage</subject><subject>Neuroglia - immunology</subject><subject>Neuroglia - metabolism</subject><subject>Neuroglia - pathology</subject><subject>Neurons - chemistry</subject><subject>Neurons - metabolism</subject><subject>Neurons - pathology</subject><subject>Protein Isoforms - biosynthesis</subject><subject>Protein Isoforms - immunology</subject><subject>Protein Isoforms - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Receptors, Antigen, T-Cell, alpha-beta - biosynthesis</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord - pathology</subject><subject>Up-Regulation</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkTtv3DAQhIkgQXyx_RcMVq4smQ9RojoHhp0YOCCNe4IiVzgeJFIhKT_-vXm4C1K62uabnd0ZhK4oqSmh7e2-3ntYY3BzzQgRNeE1of0XtKGyY5VsGP2KNgUUleiYPEM_UtoTQgVv-u_ojIqeiYbyDVof3pYIKbngcRix0S8QJucreoMrdoO1t7ji2Hmcd4DT4ryesAnRpgO9hVeXcNQ54VeXdxjeFohuBp8LpddcrptXDxi8gWWnpzC_w-SySxfo26inBJeneY6eHx-e739X2z-_nu5_bivD-y5XI-NgCYNuZEBaSqEZuWYt11oPAzdtRwY6cG6lFE2nCbS664kd7SikNbLn5-j6uHaJ4e8KKavZJQPTpD2ENalWlsxE034K0o4LJiUvYHsETQwpRRjVUh7W8V1Rog7FqL36V4w6FKMIV8WkCK9ODuswg_0vOzVRgLsjACWPFwdRJeMOwVkXwWRlg_vM4wOYBqPf</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>Shin, Taekyun</creator><creator>Kim, Heechul</creator><creator>Jin, Jae-kwang</creator><creator>Moon, Changjong</creator><creator>Ahn, Meejung</creator><creator>Tanuma, Naoyuki</creator><creator>Matsumoto, Yoh</creator><general>Elsevier B.V</general><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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20050801</creationdate><title>Expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis</title><author>Shin, Taekyun ; Kim, Heechul ; Jin, Jae-kwang ; Moon, Changjong ; Ahn, Meejung ; Tanuma, Naoyuki ; Matsumoto, Yoh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c397t-f23ed02e7f2e0611e4f3a263aaabb3c670b1b33d88547a0e6a790dfdf58dc893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Astrocyte</topic><topic>Caveolin</topic><topic>Caveolin 1</topic><topic>Caveolin 2</topic><topic>Caveolin 3</topic><topic>Caveolins - biosynthesis</topic><topic>Caveolins - immunology</topic><topic>Caveolins - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Experimental autoimmune encephalomyelitis</topic><topic>Female</topic><topic>Immune Sera</topic><topic>Immunohistochemistry</topic><topic>Immunophenotyping</topic><topic>Microglia/macrophage</topic><topic>Neuroglia - immunology</topic><topic>Neuroglia - metabolism</topic><topic>Neuroglia - pathology</topic><topic>Neurons - chemistry</topic><topic>Neurons - metabolism</topic><topic>Neurons - pathology</topic><topic>Protein Isoforms - biosynthesis</topic><topic>Protein Isoforms - immunology</topic><topic>Protein Isoforms - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Receptors, Antigen, T-Cell, alpha-beta - biosynthesis</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord - pathology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Taekyun</creatorcontrib><creatorcontrib>Kim, Heechul</creatorcontrib><creatorcontrib>Jin, Jae-kwang</creatorcontrib><creatorcontrib>Moon, Changjong</creatorcontrib><creatorcontrib>Ahn, Meejung</creatorcontrib><creatorcontrib>Tanuma, Naoyuki</creatorcontrib><creatorcontrib>Matsumoto, Yoh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Taekyun</au><au>Kim, Heechul</au><au>Jin, Jae-kwang</au><au>Moon, Changjong</au><au>Ahn, Meejung</au><au>Tanuma, Naoyuki</au><au>Matsumoto, Yoh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>165</volume><issue>1</issue><spage>11</spage><epage>20</epage><pages>11-20</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>The expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis (EAE) was analyzed. Western blot analysis showed that three isotypes of caveolins including caveolin-1, -2 and -3 increased significantly in the spinal cords of rats during the early stage of EAE, as compared with the levels in control animals (
p
<
0.05); the elevated level of each caveolin persisted during the peak and recovery stage of EAE. Immunohistochemistry demonstrated that caveolin-1 and -2 were expressed constitutively in the vascular endothelial cells and ependymal cells of the normal rat spinal cord, whereas caveolin-3 was almost exclusively localized in astrocytes. In EAE lesions, the immunoreactivity of caveolin-1 was increased in the ependymal cells, some astrocytes, and some inflammatory cells of the spinal cord, while that of caveolin-2 showed an intense immunoreactivity. Caveolin-3 was expressed constitutively in some astrocytes, but not in endothelial cells; its immunoreactivity was increased in reactive astrocytes in EAE lesions. The results of the Western blot analysis largely confirmed the observations obtained with immunohistochemistry.
Taking all the findings into consideration, we postulate that the expression levels of each caveolin begin to increase when EAE is initiated, possibly contributing to the modulation of signal transduction pathways in the affected cells.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>15925413</pmid><doi>10.1016/j.jneuroim.2005.03.019</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Astrocyte Caveolin Caveolin 1 Caveolin 2 Caveolin 3 Caveolins - biosynthesis Caveolins - immunology Caveolins - metabolism Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Experimental autoimmune encephalomyelitis Female Immune Sera Immunohistochemistry Immunophenotyping Microglia/macrophage Neuroglia - immunology Neuroglia - metabolism Neuroglia - pathology Neurons - chemistry Neurons - metabolism Neurons - pathology Protein Isoforms - biosynthesis Protein Isoforms - immunology Protein Isoforms - metabolism Rats Rats, Inbred Lew Receptors, Antigen, T-Cell, alpha-beta - biosynthesis Spinal Cord - metabolism Spinal Cord - pathology Up-Regulation |
| title | Expression of caveolin-1, -2, and -3 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis |
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