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- Publisher Website: 10.1523/JNEUROSCI.3734-15.2016
- Scopus: eid_2-s2.0-84966564957
- PMID: 27170118
- WOS: WOS:000378279500003
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Article: Caveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis
Title | Caveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis |
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Authors | |
Keywords | Caveolin-1 Experimental autoimmune encephalomyelitis ICAM-1 Lymphocyte trafficking VCAM-1 |
Issue Date | 2016 |
Publisher | Society for Neuroscience. The Journal's web site is located at http://www.jneurosci.org |
Citation | The Journal of Neuroscience, 2016, v. 36 n. 19, p. 5193-5199 How to Cite? |
Abstract | Multiple sclerosis (MS) is a progressive autoimmune disease of the CNS with its underlying mechanisms not fully understood. In the present study, we tested the hypothesis that caveolin-1, a major membrane scaffolding protein, plays a critical role in the pathogenesis of experimental autoimmune encephalomyelitis, a laboratory murine model of MS. We found increased expression of caveolin-1 in serum and spinal cord tissues in association with disease incidence and severity in wild-type mice with active encephalomyelitis. After immunization, Cav-1 knock-out mice showed remarkable disease resistance with decreased incidence and clinical symptoms. Furthermore, Cav-1 knock-out mice had alleviated encephalitogenic T cells trafficking into the CNS with decreased expressions of adhesion molecules ICAM-1 and VCAM-1 within the lesions. In agreement with in vivo studies, in vitro knockdown of caveolin-1 compromised the upregulation of ICAM-1 in endothelial cells, leading to the amelioration of the transendothelial migration of pathogenic TH1 and TH17 cells. Together, those results indicate that caveolin-1 serves as an active modulator of CNS-directed lymphocyte trafficking and could be a therapeutic target for neuroinflammatory diseases, such as multiple sclerosis. |
Persistent Identifier | http://hdl.handle.net/10722/228951 |
ISSN | 2023 Impact Factor: 4.4 2023 SCImago Journal Rankings: 2.321 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | WU, H | - |
dc.contributor.author | Deng, R | - |
dc.contributor.author | Chen, X | - |
dc.contributor.author | Wong, WM | - |
dc.contributor.author | Chen, H | - |
dc.contributor.author | Gao, L | - |
dc.contributor.author | Ni, YC | - |
dc.contributor.author | Wu, W | - |
dc.contributor.author | Shen, J | - |
dc.date.accessioned | 2016-08-23T14:08:03Z | - |
dc.date.available | 2016-08-23T14:08:03Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | The Journal of Neuroscience, 2016, v. 36 n. 19, p. 5193-5199 | - |
dc.identifier.issn | 0270-6474 | - |
dc.identifier.uri | http://hdl.handle.net/10722/228951 | - |
dc.description.abstract | Multiple sclerosis (MS) is a progressive autoimmune disease of the CNS with its underlying mechanisms not fully understood. In the present study, we tested the hypothesis that caveolin-1, a major membrane scaffolding protein, plays a critical role in the pathogenesis of experimental autoimmune encephalomyelitis, a laboratory murine model of MS. We found increased expression of caveolin-1 in serum and spinal cord tissues in association with disease incidence and severity in wild-type mice with active encephalomyelitis. After immunization, Cav-1 knock-out mice showed remarkable disease resistance with decreased incidence and clinical symptoms. Furthermore, Cav-1 knock-out mice had alleviated encephalitogenic T cells trafficking into the CNS with decreased expressions of adhesion molecules ICAM-1 and VCAM-1 within the lesions. In agreement with in vivo studies, in vitro knockdown of caveolin-1 compromised the upregulation of ICAM-1 in endothelial cells, leading to the amelioration of the transendothelial migration of pathogenic TH1 and TH17 cells. Together, those results indicate that caveolin-1 serves as an active modulator of CNS-directed lymphocyte trafficking and could be a therapeutic target for neuroinflammatory diseases, such as multiple sclerosis. | - |
dc.language | eng | - |
dc.publisher | Society for Neuroscience. The Journal's web site is located at http://www.jneurosci.org | - |
dc.relation.ispartof | The Journal of Neuroscience | - |
dc.rights | The Journal of Neuroscience. Copyright © Society for Neuroscience. | - |
dc.subject | Caveolin-1 | - |
dc.subject | Experimental autoimmune encephalomyelitis | - |
dc.subject | ICAM-1 | - |
dc.subject | Lymphocyte trafficking | - |
dc.subject | VCAM-1 | - |
dc.title | Caveolin-1 Is Critical for Lymphocyte Trafficking into Central Nervous System during Experimental Autoimmune Encephalomyelitis | - |
dc.type | Article | - |
dc.identifier.email | Deng, R: rxdeng@hku.hk | - |
dc.identifier.email | Chen, X: chenxm@hku.hk | - |
dc.identifier.email | Wong, WM: wmwonga@hku.hk | - |
dc.identifier.email | Chen, H: chenhs@hku.hk | - |
dc.identifier.email | Wu, W: wtwu@hkucc.hku.hk | - |
dc.identifier.email | Shen, J: shenjg@hku.hk | - |
dc.identifier.authority | Wu, W=rp00419 | - |
dc.identifier.authority | Shen, J=rp00487 | - |
dc.identifier.doi | 10.1523/JNEUROSCI.3734-15.2016 | - |
dc.identifier.pmid | 27170118 | - |
dc.identifier.scopus | eid_2-s2.0-84966564957 | - |
dc.identifier.hkuros | 261525 | - |
dc.identifier.volume | 36 | - |
dc.identifier.issue | 19 | - |
dc.identifier.spage | 5193 | - |
dc.identifier.epage | 5199 | - |
dc.identifier.isi | WOS:000378279500003 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0270-6474 | - |