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Conference Paper: Akt (Protein Kinase B) subtypes in retinal ischemic postconditioning

TitleAkt (Protein Kinase B) subtypes in retinal ischemic postconditioning
Authors
Issue Date2010
PublisherAmerican Society Anesthesiologists (ASA)
Citation
The 2010 Annual Meeting of the American Society Anesthesiologists (ASA), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. A1041 How to Cite?
AbstractINTRODUCTION: We have previously described enhancement of recovery in a rat model of retinal ischemia by ischemic post-conditioning using transient elevation of intraocular pressure after ischemia. We previously demonstrated involvement of protein kinase B (Akt) in this form of neuroprotection. In this study, we examined the hypothesis that specific Akt subtypes underlie this phenomenon. METHODS: Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure for 55 min in anesthetized adult Wistar rats. Post-conditioning was produced by 8 min elevation of intraocular pressure to the same level at 5 min after reperfusion following ischemia. Interfering RNA (siRNA) to Akt subtypes 1, 2, or 3, or non-silencing siRNA was injected into the vitreous 6 h prior to ischemia. Recovery was assessed using electroretinography (ERG) and histological examination of 5-micron thick retinal paraffin embedded sections. RESULTS: Injection of interfering RNA to Akt subtype 1 significantly decreased the post-conditioning ischemia protective effect as reflected by decreased recovery of the electroretinogram b wave and oscillatory potentials (OPs) (Figure).[figure1]CONCLUSIONS: The results show the involvement of specific Akt subtypes in the intriguing and clinically relevant phenomenon of post-ischemic conditioning. Enhancing expression of these subtypes may be a viable means to decrease neuronal injury after ischemia.
DescriptionTopic: Experimental Neurosciences
Persistent Identifierhttp://hdl.handle.net/10722/141240

 

DC FieldValueLanguage
dc.contributor.authorRoth, Sen_US
dc.contributor.authorDreixler, JCen_US
dc.contributor.authorShaikh, ARen_US
dc.contributor.authorAlexander, Men_US
dc.contributor.authorMarcet, Men_US
dc.date.accessioned2011-09-23T06:28:52Z-
dc.date.available2011-09-23T06:28:52Z-
dc.date.issued2010en_US
dc.identifier.citationThe 2010 Annual Meeting of the American Society Anesthesiologists (ASA), San Diego, CA., 16-20 October 2010. In Conference Proceedings, 2010, abstract no. A1041en_US
dc.identifier.urihttp://hdl.handle.net/10722/141240-
dc.descriptionTopic: Experimental Neurosciences-
dc.description.abstractINTRODUCTION: We have previously described enhancement of recovery in a rat model of retinal ischemia by ischemic post-conditioning using transient elevation of intraocular pressure after ischemia. We previously demonstrated involvement of protein kinase B (Akt) in this form of neuroprotection. In this study, we examined the hypothesis that specific Akt subtypes underlie this phenomenon. METHODS: Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure for 55 min in anesthetized adult Wistar rats. Post-conditioning was produced by 8 min elevation of intraocular pressure to the same level at 5 min after reperfusion following ischemia. Interfering RNA (siRNA) to Akt subtypes 1, 2, or 3, or non-silencing siRNA was injected into the vitreous 6 h prior to ischemia. Recovery was assessed using electroretinography (ERG) and histological examination of 5-micron thick retinal paraffin embedded sections. RESULTS: Injection of interfering RNA to Akt subtype 1 significantly decreased the post-conditioning ischemia protective effect as reflected by decreased recovery of the electroretinogram b wave and oscillatory potentials (OPs) (Figure).[figure1]CONCLUSIONS: The results show the involvement of specific Akt subtypes in the intriguing and clinically relevant phenomenon of post-ischemic conditioning. Enhancing expression of these subtypes may be a viable means to decrease neuronal injury after ischemia.-
dc.languageengen_US
dc.publisherAmerican Society Anesthesiologists (ASA)en_US
dc.relation.ispartofAnnual Meeting of the American Society Anesthesiologists, ASA 2010 Proceedingsen_US
dc.titleAkt (Protein Kinase B) subtypes in retinal ischemic postconditioningen_US
dc.typeConference_Paperen_US
dc.identifier.emailMarcet, M: marcet@hku.hken_US
dc.identifier.authorityMarcet, M=rp01363en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros194469en_US
dc.publisher.placeUnited States-

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