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Article: Intravenously administered BMSCs reduce neuronal apoptosis and promote neuronal proliferation through the release of VEGF after stroke in rats

TitleIntravenously administered BMSCs reduce neuronal apoptosis and promote neuronal proliferation through the release of VEGF after stroke in rats
Authors
Issue Date2010
PublisherManey Publishing. The Journal's web site is located at http://www.maney.co.uk/search?fwaction=show&fwid=503
Citation
Neurological Research, 2010, v. 32 n. 2, p. 148-156 How to Cite?
AbstractBackground: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) could ameliorate neurological deficits after stroke in the rodent. Objective: The purpose of this study was to investigate the potential mechanisms underlying the neuroprotective effects of implanted BMSCs. Methods: Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAo) in Sprague-Dawley rats. BMSCs were intravenously transplanted at 24 hours after MCAo. Neurological function was evaluated using modified neurological severity score and Morris water maze test. Immunohistochemistry and terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining were performed to detect neuronal apoptosis and proliferation. The protein and mRNA levels of vascular endothelial growth factor (VEGF) were determined by ELISA and reverse transcriptase polymerase chain reaction, respectively. Results: Significant improvement of neurological deficits was found in BMSC-treated rats compared with control animals at 14 and 28 days after MCAo (p<0.05). Histological evaluation showed that BMSCs treatment significantly promoted neuronal survival and proliferation in the ischemic boundary area. The expression of VEGF was predominantly increased in the ischemic hemisphere of BMSC-treated rats compared with the other groups. On the other hand, transduction of VEGF RNAi lentivirus partially attenuated the above described beneficial effects of systemically administered BMSCs. Conclusion: Our data suggest that intravenously administrated BMSCs facilitate neurological function, reduce neuronal apoptosis and promote neuronal proliferation through the release of VEGF. © 2010 W.S. Maney & Son Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/170156
ISSN
2015 Impact Factor: 1.418
2015 SCImago Journal Rankings: 0.753
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDeng, YBen_US
dc.contributor.authorYe, WBen_US
dc.contributor.authorHu, ZZen_US
dc.contributor.authorYan, Yen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorTakon, BFen_US
dc.contributor.authorZhou, GQen_US
dc.contributor.authorZhou, YFen_US
dc.date.accessioned2012-10-30T06:05:41Z-
dc.date.available2012-10-30T06:05:41Z-
dc.date.issued2010en_US
dc.identifier.citationNeurological Research, 2010, v. 32 n. 2, p. 148-156en_US
dc.identifier.issn0161-6412en_US
dc.identifier.urihttp://hdl.handle.net/10722/170156-
dc.description.abstractBackground: Transplantation of bone marrow-derived mesenchymal stem cells (BMSCs) could ameliorate neurological deficits after stroke in the rodent. Objective: The purpose of this study was to investigate the potential mechanisms underlying the neuroprotective effects of implanted BMSCs. Methods: Ischemic stroke was induced by permanent middle cerebral artery occlusion (MCAo) in Sprague-Dawley rats. BMSCs were intravenously transplanted at 24 hours after MCAo. Neurological function was evaluated using modified neurological severity score and Morris water maze test. Immunohistochemistry and terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling staining were performed to detect neuronal apoptosis and proliferation. The protein and mRNA levels of vascular endothelial growth factor (VEGF) were determined by ELISA and reverse transcriptase polymerase chain reaction, respectively. Results: Significant improvement of neurological deficits was found in BMSC-treated rats compared with control animals at 14 and 28 days after MCAo (p<0.05). Histological evaluation showed that BMSCs treatment significantly promoted neuronal survival and proliferation in the ischemic boundary area. The expression of VEGF was predominantly increased in the ischemic hemisphere of BMSC-treated rats compared with the other groups. On the other hand, transduction of VEGF RNAi lentivirus partially attenuated the above described beneficial effects of systemically administered BMSCs. Conclusion: Our data suggest that intravenously administrated BMSCs facilitate neurological function, reduce neuronal apoptosis and promote neuronal proliferation through the release of VEGF. © 2010 W.S. Maney & Son Ltd.en_US
dc.languageengen_US
dc.publisherManey Publishing. The Journal's web site is located at http://www.maney.co.uk/search?fwaction=show&fwid=503en_US
dc.relation.ispartofNeurological Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Physiologyen_US
dc.subject.meshApoptosis Regulatory Proteins - Secretionen_US
dc.subject.meshBone Marrow Cells - Secretionen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshInfusions, Intravenousen_US
dc.subject.meshMaleen_US
dc.subject.meshMesenchymal Stem Cell Transplantation - Methodsen_US
dc.subject.meshNeurons - Pathology - Secretionen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshStroke - Metabolism - Pathology - Surgeryen_US
dc.subject.meshVascular Endothelial Growth Factor A - Secretionen_US
dc.titleIntravenously administered BMSCs reduce neuronal apoptosis and promote neuronal proliferation through the release of VEGF after stroke in ratsen_US
dc.typeArticleen_US
dc.identifier.emailZhou, GQ:wormoscz@gmail.comen_US
dc.identifier.authorityZhou, GQ=rp00527en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1179/174313209X414434en_US
dc.identifier.pmid19473555-
dc.identifier.scopuseid_2-s2.0-77949470463en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77949470463&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume32en_US
dc.identifier.issue2en_US
dc.identifier.spage148en_US
dc.identifier.epage156en_US
dc.identifier.isiWOS:000274781900008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridDeng, YB=15032713100en_US
dc.identifier.scopusauthoridYe, WB=26027683200en_US
dc.identifier.scopusauthoridHu, ZZ=36522678400en_US
dc.identifier.scopusauthoridYan, Y=15081728000en_US
dc.identifier.scopusauthoridWang, Y=23394316400en_US
dc.identifier.scopusauthoridTakon, BF=35747288800en_US
dc.identifier.scopusauthoridZhou, GQ=23394245100en_US
dc.identifier.scopusauthoridZhou, YF=14038475300en_US
dc.identifier.citeulike6840168-

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