ArticleExperimental eye research2009
The role of Akt/protein kinase B subtypes in retinal ischemic preconditioning.
Article in Experimental eye research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Protective effects of blocking PD-1 pathway on retinal ganglion cells in a mouse model of chronic ocular hypertension.Frontiers in immunology · 2022Article
- Caffeine exposure ameliorates acute ischemic cell death in avian developing retina.Purinergic signalling · 2020Article
- Adaptive Plasticity in the Retina: Protection Against Acute Injury and Neurodegenerative Disease by Conditioning Stimuli.Conditioning medicine · 2018Article
- PI3K/Akt Pathway: A Role in δ-Opioid Receptor-Mediated RGC Neuroprotection.Investigative ophthalmology & visual science · 2017Article
- Bone-marrow mesenchymal stem-cell administration significantly improves outcome after retinal ischemia in rats.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2017Article
- The Protective Role of PAC1-Receptor Agonist Maxadilan in BCCAO-Induced Retinal Degeneration.Journal of molecular neuroscience : MN · 2016Article
- Induction of ischemic tolerance as a promising treatment against diabetic retinopathy.Neural regeneration research · 2014Review
- Delayed administration of bone marrow mesenchymal stem cell conditioned medium significantly improves outcome after retinal ischemia in rats.Investigative ophthalmology & visual science · 2014Article
- The Akt1 isoform is an essential mediator of ischaemic preconditioning.Journal of cellular and molecular medicine · 2012Article
- Docosahexaenoic acid pretreatment confers protection and functional improvements after acute spinal cord injury in adult rats.Journal of neurotrauma · 2012Article
- β1 integrin-focal adhesion kinase (FAK) signaling modulates retinal ganglion cell (RGC) survival.PloS one · 2012Article
- Protein kinase B (Akt) and mitogen-activated protein kinase p38α in retinal ischemic post-conditioning.Journal of molecular neuroscience : MN · 2011Article
- Mitogen-activated protein kinase phosphatase-1 (MKP-1) in retinal ischemic preconditioning.Experimental eye research · 2011Article
- Delayed post-ischemic conditioning significantly improves the outcome after retinal ischemia.Experimental eye research · 2011Article
- Novel avenues of drug discovery and biomarkers for diabetes mellitus.Journal of clinical pharmacology · 2011Review
- Post-ischemic conditioning in the rat retina is dependent upon ischemia duration and is not additive with ischemic pre-conditioning.Experimental eye research · 2010Article
- Diabetes mellitus: channeling care through cellular discovery.Current neurovascular research · 2010Article
- Mitogen-activated protein kinase p38alpha and retinal ischemic preconditioning.Experimental eye research · 2009Article
- Wnt1 neuroprotection translates into improved neurological function during oxidant stress and cerebral ischemia through AKT1 and mitochondrial apoptotic pathways.Oxidative medicine and cellular longevityArticle
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Potent endogenous protection from ischemia can be induced in the retina by ischemic preconditioning (IPC). Protein kinase B/Akt is a cellular survival factor. We hypothesized that Akt was integral to IPC based upon differential effects of Akt subtypes. Rats were subjected to retinal ischemia after IPC or IPC-mimicking by the opening of mitochondrial KATP (mKATP) channels. The effects of blocking Akt using wortmannin, API-2, or small interfering RNA (siRNA) were examined. Electroretinography assessed functional recovery after ischemia, and TUNEL examined retinal ganglion cell apoptosis. We studied the relationship between Akt activation and known initiators of IPC, including adenosine receptor stimulation and the opening of mKATP channels. The PI-3 kinase inhibitor wortmannin 1 or 4 mg/kg (i.p.), the specific Akt inhibitor API-2, 5-500 microM in the vitreous, or intravitreal siRNA directed against Akt2 or -3, but not Akt1, significantly attenuated the neuroprotective effect of IPC. Interfering RNA against any of the three Akt subtypes significantly but time-dependently attenuated mKATP channel opening to mimic IPC. Adenosine A1 receptor blockade (DPCPX), A2a blockade (CSC), or the mKATP channel blocker 5-hydroxydecanoic acid significantly attenuated Akt activation after IPC. Interfering RNA directed against Akt subtypes prevented the ameliorative effect of IPC on post-ischemic apoptosis. All three Akt subtypes are involved in functional retinal neuroprotection by IPC or IPC-mimicking. Akt is downstream of adenosine A1 and A2a receptors and mKATP channel opening. The results indicate the presence in the retina of robust and redundant endogenous neuroprotection based upon subtypes of Akt.
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