Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury
Traumatic spinal cord injury (SCI) causes tissue loss and associated neurological dysfunction attributable to both mechanical damage and secondary biochemical and physiological responses. Upregulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these change...
Gespeichert in:
Veröffentlicht in: | Molecular neurobiology 2016-11, Vol.53 (9), p.6043 |
---|---|
Hauptverfasser: | , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | |
---|---|
container_issue | 9 |
container_start_page | 6043 |
container_title | Molecular neurobiology |
container_volume | 53 |
creator | Chen, Min-hao Liu, Yong-hua Xu, Hua Xu, Da-wei Wang, Cheng-niu Wang, Yi Duan, Cheng-wei Zhou, Ying Kan, Peng Shen, Ai-guo Wang, You-hua |
description | Traumatic spinal cord injury (SCI) causes tissue loss and associated neurological dysfunction attributable to both mechanical damage and secondary biochemical and physiological responses. Upregulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these changes. Increased cell cycle protein is associated with neuronal and oligodendroglial apoptosis, reactive astrogliosis, glial scar formation, and microglial activation. Here, using lentiviral vectors (LV), we induced the expression of the cyclin-dependent kinase (CDK) inhibitor p27kip1 in the lesioned spinal cord of adult rat. Treatment with LV-p27kip1 significantly reduced the expression of cell cycle proteins and improved functional recovery. In addition, p27kip1 overexpression also reduced lesion volume, decreased astrocytic reactivity, attenuated microglial activation, reduced cell death, and improved the local microenvironment. We suggest that these effects reflect the ability of p27kip1 to inhibit cell cycle pathways. Thus, the present study provides further support for the therapeutic potential of cell cycle inhibitors in the treatment of SCI. |
doi_str_mv | 10.1007/s12035-015-9498-2 |
format | Article |
fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_1833159163</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>4231326821</sourcerecordid><originalsourceid>FETCH-proquest_journals_18331591633</originalsourceid><addsrcrecordid>eNqNjMFKAzEUAEOx0NX6Ad4CnqN5SdNNjlJaLOhFxWNL2H2FrMsm5mWL_Xv34Ad4msvMMHYH8gGkrB8JlNRGSDDCrZwVasYqMMYJAKuuWCWt06Jer-yCXRN1UioFsq6Yf8GhhHPIvuef2JSYxSu2wRdseVL1gcbEv0KCA9_-pIxEIQ5855vQhzJJxN-wiWfMF_50Kpj5ewrDtNrE3PL90I35smTzk-8Jb_94w-5324_Ns0g5fo9I5djFMU8RHcFqDcbBWuv_Wb8ppkt8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1833159163</pqid></control><display><type>article</type><title>Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury</title><source>Springer Nature - Complete Springer Journals</source><creator>Chen, Min-hao ; Liu, Yong-hua ; Xu, Hua ; Xu, Da-wei ; Wang, Cheng-niu ; Wang, Yi ; Duan, Cheng-wei ; Zhou, Ying ; Kan, Peng ; Shen, Ai-guo ; Wang, You-hua</creator><creatorcontrib>Chen, Min-hao ; Liu, Yong-hua ; Xu, Hua ; Xu, Da-wei ; Wang, Cheng-niu ; Wang, Yi ; Duan, Cheng-wei ; Zhou, Ying ; Kan, Peng ; Shen, Ai-guo ; Wang, You-hua</creatorcontrib><description>Traumatic spinal cord injury (SCI) causes tissue loss and associated neurological dysfunction attributable to both mechanical damage and secondary biochemical and physiological responses. Upregulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these changes. Increased cell cycle protein is associated with neuronal and oligodendroglial apoptosis, reactive astrogliosis, glial scar formation, and microglial activation. Here, using lentiviral vectors (LV), we induced the expression of the cyclin-dependent kinase (CDK) inhibitor p27kip1 in the lesioned spinal cord of adult rat. Treatment with LV-p27kip1 significantly reduced the expression of cell cycle proteins and improved functional recovery. In addition, p27kip1 overexpression also reduced lesion volume, decreased astrocytic reactivity, attenuated microglial activation, reduced cell death, and improved the local microenvironment. We suggest that these effects reflect the ability of p27kip1 to inhibit cell cycle pathways. Thus, the present study provides further support for the therapeutic potential of cell cycle inhibitors in the treatment of SCI.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-015-9498-2</identifier><language>eng</language><publisher>Totowa: Springer Nature B.V</publisher><subject>Apoptosis ; Cell cycle ; Cell growth ; Neurobiology ; Spinal cord injuries</subject><ispartof>Molecular neurobiology, 2016-11, Vol.53 (9), p.6043</ispartof><rights>Springer Science+Business Media New York 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Chen, Min-hao</creatorcontrib><creatorcontrib>Liu, Yong-hua</creatorcontrib><creatorcontrib>Xu, Hua</creatorcontrib><creatorcontrib>Xu, Da-wei</creatorcontrib><creatorcontrib>Wang, Cheng-niu</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Duan, Cheng-wei</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Kan, Peng</creatorcontrib><creatorcontrib>Shen, Ai-guo</creatorcontrib><creatorcontrib>Wang, You-hua</creatorcontrib><title>Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury</title><title>Molecular neurobiology</title><description>Traumatic spinal cord injury (SCI) causes tissue loss and associated neurological dysfunction attributable to both mechanical damage and secondary biochemical and physiological responses. Upregulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these changes. Increased cell cycle protein is associated with neuronal and oligodendroglial apoptosis, reactive astrogliosis, glial scar formation, and microglial activation. Here, using lentiviral vectors (LV), we induced the expression of the cyclin-dependent kinase (CDK) inhibitor p27kip1 in the lesioned spinal cord of adult rat. Treatment with LV-p27kip1 significantly reduced the expression of cell cycle proteins and improved functional recovery. In addition, p27kip1 overexpression also reduced lesion volume, decreased astrocytic reactivity, attenuated microglial activation, reduced cell death, and improved the local microenvironment. We suggest that these effects reflect the ability of p27kip1 to inhibit cell cycle pathways. Thus, the present study provides further support for the therapeutic potential of cell cycle inhibitors in the treatment of SCI.</description><subject>Apoptosis</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Neurobiology</subject><subject>Spinal cord injuries</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqNjMFKAzEUAEOx0NX6Ad4CnqN5SdNNjlJaLOhFxWNL2H2FrMsm5mWL_Xv34Ad4msvMMHYH8gGkrB8JlNRGSDDCrZwVasYqMMYJAKuuWCWt06Jer-yCXRN1UioFsq6Yf8GhhHPIvuef2JSYxSu2wRdseVL1gcbEv0KCA9_-pIxEIQ5855vQhzJJxN-wiWfMF_50Kpj5ewrDtNrE3PL90I35smTzk-8Jb_94w-5324_Ns0g5fo9I5djFMU8RHcFqDcbBWuv_Wb8ppkt8</recordid><startdate>20161101</startdate><enddate>20161101</enddate><creator>Chen, Min-hao</creator><creator>Liu, Yong-hua</creator><creator>Xu, Hua</creator><creator>Xu, Da-wei</creator><creator>Wang, Cheng-niu</creator><creator>Wang, Yi</creator><creator>Duan, Cheng-wei</creator><creator>Zhou, Ying</creator><creator>Kan, Peng</creator><creator>Shen, Ai-guo</creator><creator>Wang, You-hua</creator><general>Springer Nature B.V</general><scope>3V.</scope><scope>7QR</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20161101</creationdate><title>Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury</title><author>Chen, Min-hao ; Liu, Yong-hua ; Xu, Hua ; Xu, Da-wei ; Wang, Cheng-niu ; Wang, Yi ; Duan, Cheng-wei ; Zhou, Ying ; Kan, Peng ; Shen, Ai-guo ; Wang, You-hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_18331591633</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Apoptosis</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Neurobiology</topic><topic>Spinal cord injuries</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Min-hao</creatorcontrib><creatorcontrib>Liu, Yong-hua</creatorcontrib><creatorcontrib>Xu, Hua</creatorcontrib><creatorcontrib>Xu, Da-wei</creatorcontrib><creatorcontrib>Wang, Cheng-niu</creatorcontrib><creatorcontrib>Wang, Yi</creatorcontrib><creatorcontrib>Duan, Cheng-wei</creatorcontrib><creatorcontrib>Zhou, Ying</creatorcontrib><creatorcontrib>Kan, Peng</creatorcontrib><creatorcontrib>Shen, Ai-guo</creatorcontrib><creatorcontrib>Wang, You-hua</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Min-hao</au><au>Liu, Yong-hua</au><au>Xu, Hua</au><au>Xu, Da-wei</au><au>Wang, Cheng-niu</au><au>Wang, Yi</au><au>Duan, Cheng-wei</au><au>Zhou, Ying</au><au>Kan, Peng</au><au>Shen, Ai-guo</au><au>Wang, You-hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury</atitle><jtitle>Molecular neurobiology</jtitle><date>2016-11-01</date><risdate>2016</risdate><volume>53</volume><issue>9</issue><spage>6043</spage><pages>6043-</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>Traumatic spinal cord injury (SCI) causes tissue loss and associated neurological dysfunction attributable to both mechanical damage and secondary biochemical and physiological responses. Upregulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these changes. Increased cell cycle protein is associated with neuronal and oligodendroglial apoptosis, reactive astrogliosis, glial scar formation, and microglial activation. Here, using lentiviral vectors (LV), we induced the expression of the cyclin-dependent kinase (CDK) inhibitor p27kip1 in the lesioned spinal cord of adult rat. Treatment with LV-p27kip1 significantly reduced the expression of cell cycle proteins and improved functional recovery. In addition, p27kip1 overexpression also reduced lesion volume, decreased astrocytic reactivity, attenuated microglial activation, reduced cell death, and improved the local microenvironment. We suggest that these effects reflect the ability of p27kip1 to inhibit cell cycle pathways. Thus, the present study provides further support for the therapeutic potential of cell cycle inhibitors in the treatment of SCI.</abstract><cop>Totowa</cop><pub>Springer Nature B.V</pub><doi>10.1007/s12035-015-9498-2</doi></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0893-7648 |
ispartof | Molecular neurobiology, 2016-11, Vol.53 (9), p.6043 |
issn | 0893-7648 1559-1182 |
language | eng |
recordid | cdi_proquest_journals_1833159163 |
source | Springer Nature - Complete Springer Journals |
subjects | Apoptosis Cell cycle Cell growth Neurobiology Spinal cord injuries |
title | Lentiviral Vector-Mediated p27^sup kip1^ Expression Facilitates Recovery After Spinal Cord Injury |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-14T20%3A22%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Lentiviral%20Vector-Mediated%20p27%5Esup%20kip1%5E%20Expression%20Facilitates%20Recovery%20After%20Spinal%20Cord%20Injury&rft.jtitle=Molecular%20neurobiology&rft.au=Chen,%20Min-hao&rft.date=2016-11-01&rft.volume=53&rft.issue=9&rft.spage=6043&rft.pages=6043-&rft.issn=0893-7648&rft.eissn=1559-1182&rft_id=info:doi/10.1007/s12035-015-9498-2&rft_dat=%3Cproquest%3E4231326821%3C/proquest%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1833159163&rft_id=info:pmid/&rfr_iscdi=true |