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Article: Mitogen-activated protein kinase phosphatase-1 (MKP-1) in retinal ischemic preconditioning

TitleMitogen-activated protein kinase phosphatase-1 (MKP-1) in retinal ischemic preconditioning
Authors
KeywordsDual-specificity phosphatase
Ischemia
Mitogen-activated protein kinase
MKP-1
P38
Preconditioning
Rat
Issue Date2011
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexer
Citation
Experimental Eye Research, 2011, v. 93 n. 4, p. 340-349 How to Cite?
AbstractWe previously described the phenomenon of retinal ischemic pre-conditioning (IPC) and we have shown the role of various signaling proteins in the protective pathways, including the mitogen-activated protein kinase p38. In this study we examined the role in IPC of mitogen-activated protein kinase phosphatase-1 (MKP-1), which inactivates p38. Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure in adult Wistar rats. Preconditioning was produced by transient retinal ischemia for 5 min, 24 h prior to ischemia. Small interfering RNA (siRNA) to MKP-1 or a control non-silencing siRNA, was injected into the vitreous 6 h prior to IPC. Recovery was assessed by electroretinography (ERG) and histology. The a-and b-waves, and oscillatory potentials (OPs), measured before and 1 week after ischemia, were then normalized relative to pre-ischemic baseline, and corrected for diurnal variation in the normal non-ischemic eye. The P2, or post-photoreceptor component of the ERG (which reflects function of the rod bipolar cells in the inner retina), was derived using the Hood-Birch model. MKP-1 was localized in specific retinal cells using immunohistochemistry; levels of mitogen-activated protein kinases were measured using Western blotting. Injection of siRNA to MKP-1 significantly attenuated the protective effect of IPC as reflected by decreased recovery of the electroretinogram a and b-waves and the P2 after ischemia. The injection of siRNA to MKP-1 reduced the number of cells in the retinal ganglion cell and outer nuclear layers after IPC and ischemia. Blockade of MKP-1 by siRNA also increased the activation of p38 at 24 h following IPC. MKP-1 siRNA did not alter the levels of phosphorylated jun N-terminal kinase (JNK) or extracellular signal-regulated kinase (ERK) after IPC. The results suggest the involvement of dual-specificity phosphatase MKP-1 in IPC and that MKP-1 is involved in IPC by regulating levels of activated MAPK p38. © 2010 Elsevier Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/141084
ISSN
2015 Impact Factor: 2.998
2015 SCImago Journal Rankings: 1.218
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of Health (Rockville, MD)RO1 EY10343-15S1
Pritzker School of MedicineAG029795-02
University of Chicago Institute for Translational MedicineUL1RR024999
Illinois Society for the Prevention of Blindness (Chicago, IL)
Dean's Research Advisory Committee of the Division of Biological Sciences of the University of Chicago
American Academy of Neurology (St Paul, MN)
Stroke Council of the American Heart Association (Dallas, TX)
Funding Information:

Supported by National Institutes of Health (Rockville, MD) grants RO1 EY10343-15S1 (American Recovery and Reinvestment Act) to Dr Roth, AG029795-02 for the Medical Student Summer Research Program at the Pritzker School of Medicine, UL1RR024999 to the University of Chicago Institute for Translational Medicine; the Illinois Society for the Prevention of Blindness (Chicago, IL); and the Dean's Research Advisory Committee of the Division of Biological Sciences of the University of Chicago. Ms Du was the recipient of a student research fellowship award from the American Academy of Neurology (St Paul, MN), and the Stroke Council of the American Heart Association (Dallas, TX).

References

 

DC FieldValueLanguage
dc.contributor.authorDreixler, JCen_HK
dc.contributor.authorBratton, Aen_HK
dc.contributor.authorDu, Een_HK
dc.contributor.authorShaikh, ARen_HK
dc.contributor.authorSavoie, Ben_HK
dc.contributor.authorAlexander, Men_HK
dc.contributor.authorMarcet, MMen_HK
dc.contributor.authorRoth, Sen_HK
dc.date.accessioned2011-09-23T06:25:11Z-
dc.date.available2011-09-23T06:25:11Z-
dc.date.issued2011en_HK
dc.identifier.citationExperimental Eye Research, 2011, v. 93 n. 4, p. 340-349en_HK
dc.identifier.issn0014-4835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/141084-
dc.description.abstractWe previously described the phenomenon of retinal ischemic pre-conditioning (IPC) and we have shown the role of various signaling proteins in the protective pathways, including the mitogen-activated protein kinase p38. In this study we examined the role in IPC of mitogen-activated protein kinase phosphatase-1 (MKP-1), which inactivates p38. Ischemia was produced by elevation of intraocular pressure above systolic arterial blood pressure in adult Wistar rats. Preconditioning was produced by transient retinal ischemia for 5 min, 24 h prior to ischemia. Small interfering RNA (siRNA) to MKP-1 or a control non-silencing siRNA, was injected into the vitreous 6 h prior to IPC. Recovery was assessed by electroretinography (ERG) and histology. The a-and b-waves, and oscillatory potentials (OPs), measured before and 1 week after ischemia, were then normalized relative to pre-ischemic baseline, and corrected for diurnal variation in the normal non-ischemic eye. The P2, or post-photoreceptor component of the ERG (which reflects function of the rod bipolar cells in the inner retina), was derived using the Hood-Birch model. MKP-1 was localized in specific retinal cells using immunohistochemistry; levels of mitogen-activated protein kinases were measured using Western blotting. Injection of siRNA to MKP-1 significantly attenuated the protective effect of IPC as reflected by decreased recovery of the electroretinogram a and b-waves and the P2 after ischemia. The injection of siRNA to MKP-1 reduced the number of cells in the retinal ganglion cell and outer nuclear layers after IPC and ischemia. Blockade of MKP-1 by siRNA also increased the activation of p38 at 24 h following IPC. MKP-1 siRNA did not alter the levels of phosphorylated jun N-terminal kinase (JNK) or extracellular signal-regulated kinase (ERK) after IPC. The results suggest the involvement of dual-specificity phosphatase MKP-1 in IPC and that MKP-1 is involved in IPC by regulating levels of activated MAPK p38. © 2010 Elsevier Ltd.en_HK
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexeren_HK
dc.relation.ispartofExperimental Eye Researchen_HK
dc.subjectDual-specificity phosphataseen_HK
dc.subjectIschemiaen_HK
dc.subjectMitogen-activated protein kinaseen_HK
dc.subjectMKP-1en_HK
dc.subjectP38en_HK
dc.subjectPreconditioningen_HK
dc.subjectRaten_HK
dc.titleMitogen-activated protein kinase phosphatase-1 (MKP-1) in retinal ischemic preconditioningen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4835&volume=93&issue=4&spage=340&epage=349&date=2010&atitle=Mitogen-activated+protein+kinase+phosphatase-1+(MKP-1)+in+retinal+ischemic+preconditioning-
dc.identifier.emailMarcet, MM: marcet@hku.hken_HK
dc.identifier.authorityMarcet, MM=rp01363en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.exer.2010.10.011en_HK
dc.identifier.pmid21094639-
dc.identifier.pmcidPMC3074007-
dc.identifier.scopuseid_2-s2.0-80054929929en_HK
dc.identifier.hkuros192921en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054929929&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume93en_HK
dc.identifier.issue4en_HK
dc.identifier.spage340en_HK
dc.identifier.epage349en_HK
dc.identifier.isiWOS:000297449900003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridDreixler, JC=6602518830en_HK
dc.identifier.scopusauthoridBratton, A=54394990200en_HK
dc.identifier.scopusauthoridDu, E=35486996900en_HK
dc.identifier.scopusauthoridShaikh, AR=7101736509en_HK
dc.identifier.scopusauthoridSavoie, B=25928801700en_HK
dc.identifier.scopusauthoridAlexander, M=37025529800en_HK
dc.identifier.scopusauthoridMarcet, MM=8891087900en_HK
dc.identifier.scopusauthoridRoth, S=7402433182en_HK
dc.identifier.citeulike8412177-

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