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Article: Protein kinase B (Akt) and mitogen-activated protein kinase p38α in retinal ischemic post-conditioning

TitleProtein kinase B (Akt) and mitogen-activated protein kinase p38α in retinal ischemic post-conditioning
Authors
KeywordsAkt
p38
Post-conditioning
Retinal ischemia
Issue Date2011
PublisherHumana Press, Inc.
Citation
Journal Of Molecular Neuroscience, 2011, v. 45 n. 2, p. 309-320 How to Cite?
AbstractIn previous studies, it was shown that post-conditioning, a transient period of brief ischemia following prolonged severe ischemia in the retina, could provide significant improvement in post-ischemic recovery, attenuation of cell loss, and decreased apoptosis. However, the mechanisms of post-conditioning in the retina have not been elucidated. We hypothesized that two kinases, mitogen-activated protein kinase p38α and protein kinase B (Akt), were involved in the mechanism of post-conditioning. Ischemia was induced in rat retina in vivo. Recovery after ischemia followed by 8 min of post-conditioning early in the reperfusion period after prolonged ischemia was assessed functionally (electroretinography) and histologically at 7 days after ischemia. We examined the role of p38α and Akt subtypes 1-3 in post-conditioning by intravitreal injection of interfering RNA 6 h prior to ischemia and post-conditioning and compared the results to injection of non-silencing interfering RNA sequence. The blockade of p38α significantly decreased the recovery after ischemia and post-conditioning, and enhanced cell loss and disorganization of the retina. Blockade of Akt1, and to a lesser degree, Akt2, significantly decreased the recovery after ischemia and enhanced cell loss and disorganization. These differences in the effects of blockade of Akt subtypes were not explainable by distribution of Akt subtypes in the retina, which were similar. In conclusion, both p38 and Akt are essential components of the neuroprotection induced by post-ischemic conditioning in the retina. © 2011 Springer Science+Business Media, LLC.
Persistent Identifierhttp://hdl.handle.net/10722/141082
ISSN
2015 Impact Factor: 2.352
2015 SCImago Journal Rankings: 0.988
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of Health (Rockville, MD)RO1 EY10343
RO1 EY10343-16S2
Pritzker School of MedicineAG029795-02
UL1RR024999
Illinois Society for the Prevention of Blindness (Chicago, IL)
Research Advisory Committee of the Division of Biological Sciences of the University of Chicago
American Academy of Neurology, St Paul, MN
Funding Information:

Supported by National Institutes of Health (Rockville, MD) grants RO1 EY10343 and RO1 EY10343-16S2 (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. Ajay Sampat was the recipient of a Medical Student Research Fellowship Award from the American Academy of Neurology, St Paul, MN. There is no conflict of interest or commercial interest for any of the authors.

References

 

DC FieldValueLanguage
dc.contributor.authorDreixler, JCen_HK
dc.contributor.authorSampat, Aen_HK
dc.contributor.authorShaikh, ARen_HK
dc.contributor.authorAlexander, Men_HK
dc.contributor.authorMarcet, MMen_HK
dc.contributor.authorRoth, Sen_HK
dc.date.accessioned2011-09-23T06:25:09Z-
dc.date.available2011-09-23T06:25:09Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Molecular Neuroscience, 2011, v. 45 n. 2, p. 309-320en_HK
dc.identifier.issn0895-8696en_HK
dc.identifier.urihttp://hdl.handle.net/10722/141082-
dc.description.abstractIn previous studies, it was shown that post-conditioning, a transient period of brief ischemia following prolonged severe ischemia in the retina, could provide significant improvement in post-ischemic recovery, attenuation of cell loss, and decreased apoptosis. However, the mechanisms of post-conditioning in the retina have not been elucidated. We hypothesized that two kinases, mitogen-activated protein kinase p38α and protein kinase B (Akt), were involved in the mechanism of post-conditioning. Ischemia was induced in rat retina in vivo. Recovery after ischemia followed by 8 min of post-conditioning early in the reperfusion period after prolonged ischemia was assessed functionally (electroretinography) and histologically at 7 days after ischemia. We examined the role of p38α and Akt subtypes 1-3 in post-conditioning by intravitreal injection of interfering RNA 6 h prior to ischemia and post-conditioning and compared the results to injection of non-silencing interfering RNA sequence. The blockade of p38α significantly decreased the recovery after ischemia and post-conditioning, and enhanced cell loss and disorganization of the retina. Blockade of Akt1, and to a lesser degree, Akt2, significantly decreased the recovery after ischemia and enhanced cell loss and disorganization. These differences in the effects of blockade of Akt subtypes were not explainable by distribution of Akt subtypes in the retina, which were similar. In conclusion, both p38 and Akt are essential components of the neuroprotection induced by post-ischemic conditioning in the retina. © 2011 Springer Science+Business Media, LLC.en_HK
dc.languageengen_US
dc.publisherHumana Press, Inc.en_US
dc.relation.ispartofJournal of Molecular Neuroscienceen_HK
dc.rightsThe original publication is available at www.springerlink.com-
dc.subjectAkten_HK
dc.subjectp38en_HK
dc.subjectPost-conditioningen_HK
dc.subjectRetinal ischemiaen_HK
dc.titleProtein kinase B (Akt) and mitogen-activated protein kinase p38α in retinal ischemic post-conditioningen_HK
dc.typeArticleen_HK
dc.identifier.emailMarcet, MM: marcet@hku.hken_HK
dc.identifier.authorityMarcet, MM=rp01363en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12031-011-9523-5en_HK
dc.identifier.pmid21573888-
dc.identifier.scopuseid_2-s2.0-80054965106en_HK
dc.identifier.hkuros192919en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80054965106&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume45en_HK
dc.identifier.issue2en_HK
dc.identifier.spage309en_HK
dc.identifier.epage320en_HK
dc.identifier.isiWOS:000295173600028-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridDreixler, JC=6602518830en_HK
dc.identifier.scopusauthoridSampat, A=35750496100en_HK
dc.identifier.scopusauthoridShaikh, AR=7101736509en_HK
dc.identifier.scopusauthoridAlexander, M=37025529800en_HK
dc.identifier.scopusauthoridMarcet, MM=8891087900en_HK
dc.identifier.scopusauthoridRoth, S=7402433182en_HK
dc.identifier.citeulike9317609-

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