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Conference Paper: Dual specificity phosphatase MKP1 and retinal ischemic preconditioning
Title | Dual specificity phosphatase MKP1 and retinal ischemic preconditioning |
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Authors | |
Issue Date | 2010 |
Publisher | American 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? |
Abstract | INTRODUCTION: 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. |
Description | Topic: Experimental Neurosciences |
Persistent Identifier | http://hdl.handle.net/10722/141241 |
DC Field | Value | Language |
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dc.contributor.author | Roth, S | en_US |
dc.contributor.author | Dreixler, JC | en_US |
dc.contributor.author | Shaikh, AR | en_US |
dc.contributor.author | Alexander, M | en_US |
dc.contributor.author | Marcet, M | en_US |
dc.date.accessioned | 2011-09-23T06:28:52Z | - |
dc.date.available | 2011-09-23T06:28:52Z | - |
dc.date.issued | 2010 | en_US |
dc.identifier.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 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/141241 | - |
dc.description | Topic: Experimental Neurosciences | - |
dc.description.abstract | INTRODUCTION: 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.language | eng | en_US |
dc.publisher | American Society Anesthesiologists (ASA). | en_US |
dc.relation.ispartof | Annual Meeting of the American Society Anesthesiologists, ASA 2010 Proceedings | en_US |
dc.title | Dual specificity phosphatase MKP1 and retinal ischemic preconditioning | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Marcet, M: marcet@hku.hk | en_US |
dc.identifier.authority | Marcet, M=rp01363 | en_US |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.hkuros | 194470 | en_US |
dc.publisher.place | United States | - |