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Conference Paper: Dual specificity phosphatase MKP1 and retinal ischemic preconditioning

TitleDual specificity phosphatase MKP1 and retinal ischemic preconditioning
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. A1527 How to Cite?
AbstractINTRODUCTION: We previously described the phemenon of retinal ischemic preconditioning (1) and showed significant increases in the dual-specificity phosphatase MKP-1 with preconditioning (2). In this study we examined the role of MKP-1 in ischemic preconditioning and specifically, its role in regulating MAPK p38. METHODS: Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure for 55 min in anesthetized adult Wistar rats. Pre-conditioning was produced by ligating the central retinal artery for 5 min using suture occlusion, 24 h prior to ischemia. Interfering RNA (siRNA) to MKP-1 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. The a and b waves, and oscillatory potentials (OPs) were measured before and 1 week after ischemia and normalized relative to pre-ischemic baseline and corrected for diurnal variation in the normal non-ischemic eye. The P2 (which reflects function of the rod bipolar cells in the inner retina) was derived using the Hood-Birch model (3). Levels of phosphorylated MAPKs p38, ERK, and JNK were measured relative to total levels of protein at 24 h after ischemic preconditioning +/- siRNA to MPK-1 or non-silencing siRNA. RESULTS: Injection of interfering RNA to to MKP-1 significantly (P < 0.05) attenuated the protective effect of ischemic preconditoning as reflected by decreased recovery of the electroretinogram a, b wave and oscillatory potentials (OPs) and the P2 (Figure).[figure1]The blockade of MKP-1 by siRNA resulted in an increase in activation of p38 at 24 h following preconditioning to 146 +/- 7 % vs that with non-silencing siRNA (108 +/ 13%, P < 0.05). MKP-1 siRNA did not alter the levels of phosphorylated JNK or ERK after preconditioning. CONCLUSIONS: The results show the involvement of dual-specificity phosphatase MKP1 in ischemic preconditioning and suggest that MKP-1 is involved in ischemic preconditioning by regulating levels of activated MAPK p38.
DescriptionTopic: Experimental Neurosciences
Persistent Identifierhttp://hdl.handle.net/10722/141241

 

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. A1527en_US
dc.identifier.urihttp://hdl.handle.net/10722/141241-
dc.descriptionTopic: Experimental Neurosciences-
dc.description.abstractINTRODUCTION: We previously described the phemenon of retinal ischemic preconditioning (1) and showed significant increases in the dual-specificity phosphatase MKP-1 with preconditioning (2). In this study we examined the role of MKP-1 in ischemic preconditioning and specifically, its role in regulating MAPK p38. METHODS: Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure for 55 min in anesthetized adult Wistar rats. Pre-conditioning was produced by ligating the central retinal artery for 5 min using suture occlusion, 24 h prior to ischemia. Interfering RNA (siRNA) to MKP-1 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. The a and b waves, and oscillatory potentials (OPs) were measured before and 1 week after ischemia and normalized relative to pre-ischemic baseline and corrected for diurnal variation in the normal non-ischemic eye. The P2 (which reflects function of the rod bipolar cells in the inner retina) was derived using the Hood-Birch model (3). Levels of phosphorylated MAPKs p38, ERK, and JNK were measured relative to total levels of protein at 24 h after ischemic preconditioning +/- siRNA to MPK-1 or non-silencing siRNA. RESULTS: Injection of interfering RNA to to MKP-1 significantly (P < 0.05) attenuated the protective effect of ischemic preconditoning as reflected by decreased recovery of the electroretinogram a, b wave and oscillatory potentials (OPs) and the P2 (Figure).[figure1]The blockade of MKP-1 by siRNA resulted in an increase in activation of p38 at 24 h following preconditioning to 146 +/- 7 % vs that with non-silencing siRNA (108 +/ 13%, P < 0.05). MKP-1 siRNA did not alter the levels of phosphorylated JNK or ERK after preconditioning. CONCLUSIONS: The results show the involvement of dual-specificity phosphatase MKP1 in ischemic preconditioning and suggest that MKP-1 is involved in ischemic preconditioning by regulating levels of activated MAPK p38.-
dc.languageengen_US
dc.publisherAmerican Society Anesthesiologists (ASA).en_US
dc.relation.ispartofAnnual Meeting of the American Society Anesthesiologists, ASA 2010 Proceedingsen_US
dc.titleDual specificity phosphatase MKP1 and retinal ischemic preconditioningen_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.hkuros194470en_US
dc.publisher.placeUnited States-

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