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Conference Paper: The Role Of GSK3-beta Pathway In Oligodendroglial Progenitor Cell Differentiation And Remyelination After Spinal Cord Injury

TitleThe Role Of GSK3-beta Pathway In Oligodendroglial Progenitor Cell Differentiation And Remyelination After Spinal Cord Injury
Authors
Issue Date2014
PublisherResearch Centre of Heart, Brain, Hormone & Healthy Aging, Li Ka Shing Faculty of Medicine, The University of Hong Kong.
Citation
The 9th International Symposium on Healthy Aging, Hong Kong, China, 8-9 March 2014 How to Cite?
AbstractBackground: Demyelination is one of the major obstacle for axon regeneration and functional recovery after SCI. Previous research has shown that a pool of resident neural progenitor cells (NPCs) in spinal cord can be recruited to produce progeny after injury. Our preliminary study shows that lithium and noggin stimulate oligodendrocyte differentiation of adult spinal cord-derived NPC (ASCNPC) and lithium exerts its effect by inhibiting GSK3β pathway. Objectives: To examine whether GSK3β inhibition leads to oligodendroglial progenitor cell differentiation and remyelination, and functional recovery after SCI. Methods: Adult mice were subjected to contusive injury at 8th-10th thoracic level. Twenty-four hours after injury, spinal cord segments were harvested for neurosphere culture. Neurosphere cells were treated with GSK3β inhibitors ARA-014418 and lithium and cultured in differentiating medium. Two weeks after SCI, mice were treated with ARA-014418 and lithium for two weeks before the being sacrificed for myelin measurement. Basso Mouse Scale (BMS) was performed weekly after injury to monitor locomotion function. Results: ARA-014418 and lithium promote both oligodendroglial and neuronal differentiation of ASCNPCs. Injured mice treated with GSK3β inhibitors exhibit better performance in BMS. The myelinated area and volume of treated spinal cords were partially rescued by GSK3β inhibitor treatment. Conclusions: Both GSK3β inhibitors ARA-014418 and lithium are effective in promoting oligodendrocyte/neuron differentiation and functional recovery after SCI. It indicates that GSK3β is a key player in impeding SCI repair
DescriptionConference Theme: Aging with Confidence
Persistent Identifierhttp://hdl.handle.net/10722/203688

 

DC FieldValueLanguage
dc.contributor.authorPan, Yen_US
dc.contributor.authorDai, Yen_US
dc.contributor.authorCheung, MPLen_US
dc.contributor.authorYip, HKFen_US
dc.date.accessioned2014-09-19T16:11:24Z-
dc.date.available2014-09-19T16:11:24Z-
dc.date.issued2014en_US
dc.identifier.citationThe 9th International Symposium on Healthy Aging, Hong Kong, China, 8-9 March 2014en_US
dc.identifier.urihttp://hdl.handle.net/10722/203688-
dc.descriptionConference Theme: Aging with Confidence-
dc.description.abstractBackground: Demyelination is one of the major obstacle for axon regeneration and functional recovery after SCI. Previous research has shown that a pool of resident neural progenitor cells (NPCs) in spinal cord can be recruited to produce progeny after injury. Our preliminary study shows that lithium and noggin stimulate oligodendrocyte differentiation of adult spinal cord-derived NPC (ASCNPC) and lithium exerts its effect by inhibiting GSK3β pathway. Objectives: To examine whether GSK3β inhibition leads to oligodendroglial progenitor cell differentiation and remyelination, and functional recovery after SCI. Methods: Adult mice were subjected to contusive injury at 8th-10th thoracic level. Twenty-four hours after injury, spinal cord segments were harvested for neurosphere culture. Neurosphere cells were treated with GSK3β inhibitors ARA-014418 and lithium and cultured in differentiating medium. Two weeks after SCI, mice were treated with ARA-014418 and lithium for two weeks before the being sacrificed for myelin measurement. Basso Mouse Scale (BMS) was performed weekly after injury to monitor locomotion function. Results: ARA-014418 and lithium promote both oligodendroglial and neuronal differentiation of ASCNPCs. Injured mice treated with GSK3β inhibitors exhibit better performance in BMS. The myelinated area and volume of treated spinal cords were partially rescued by GSK3β inhibitor treatment. Conclusions: Both GSK3β inhibitors ARA-014418 and lithium are effective in promoting oligodendrocyte/neuron differentiation and functional recovery after SCI. It indicates that GSK3β is a key player in impeding SCI repairen_US
dc.languageengen_US
dc.publisherResearch Centre of Heart, Brain, Hormone & Healthy Aging, Li Ka Shing Faculty of Medicine, The University of Hong Kong.-
dc.relation.ispartofInternational Symposium on Healthy Aging: Aging with Confidenceen_US
dc.titleThe Role Of GSK3-beta Pathway In Oligodendroglial Progenitor Cell Differentiation And Remyelination After Spinal Cord Injuryen_US
dc.typeConference_Paperen_US
dc.identifier.emailCheung, MPL: mplcheun@hkucc.hku.hken_US
dc.identifier.emailYip, HKF: hkfyip@hku.hken_US
dc.identifier.authorityYip, HKF=rp00285en_US
dc.identifier.hkuros235287en_US
dc.publisher.placeHong Kong-

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