ArticleCell death and differentiation2014
The nitric oxide-cGKII system relays death and survival signals during embryonic retinal development via AKT-induced CREB1 activation.
Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- The Emerging Role of Phosphodiesterase 5 Inhibition in Neurological Disorders: The State of the Art.Cells · 2024Review
- The Healthy and Diseased Retina Seen through Neuron-Glia Interactions.International journal of molecular sciences · 2024Review
- A two-step Bayesian network approach to identify key SNPs associated to multiple phenotypic traits in four purebred laying hen lines.PloS one · 2024Article
- Maf1 controls retinal neuron number by both RNA Pol III- and Pol II-dependent mechanisms.iScience · 2023Article
- Chemical signaling in the developing avian retina: Focus on cyclic AMP and AKT-dependent pathways.Frontiers in cell and developmental biology · 2022Review
- miR-133a-3p promotes apoptosis and induces cell cycle arrest by targeting CREB1 in retinoblastoma.Archives of medical science : AMS · 2020Article
- Astaxanthin Inhibits Mitochondrial Permeability Transition Pore Opening in Rat Heart Mitochondria.Antioxidants (Basel, Switzerland) · 2019Article
- High hydrostatic pressure induces apoptosis of retinal ganglion cells via regulation of the NGF signalling pathway.Molecular medicine reports · 2019Article
- Structural Analysis of Hippocampal Kinase Signal Transduction.ACS chemical neuroscience · 2018Article
- Dopamine promotes NMDA receptor hypofunction in the retina through DScientific reports · 2017Article
- Propofol Enhances Hemoglobin-Induced Cytotoxicity in Neurons.Anesthesia and analgesia · 2016Article
- Astaxanthin Inhibits Acetaldehyde-Induced Cytotoxicity in SH-SY5Y Cells by Modulating Akt/CREB and p38MAPK/ERK Signaling Pathways.Marine drugs · 2016Article
- Bcl-2, Bcl-xL, and p-AKT are involved in neuroprotective effects of transcription factor Brn3b in an ocular hypertension rat model of glaucoma.Molecular vision · 2016Article
- NF-κB protects human neuroblastoma cells from nitric oxide-induced apoptosis through upregulating biglycan.American journal of translational research · 2015Article
- Akt inhibitor MK2206 prevents influenza pH1N1 virus infection in vitro.Antimicrobial agents and chemotherapy · 2014Article
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6 authors.
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Abstract
During early neurogenesis, retinal neuronal cells display a conserved differentiation program in vertebrates. Previous studies established that nitric oxide (NO) and cGMP accumulation regulate essential events in retinal physiology. Here we used pharmacological and genetic loss-of-function to investigate the effects of NO and its downstream signaling pathway in the survival of developing avian retinal neurons in vitro and in vivo. Six-day-old (E6) chick retinal cells displayed increased calcium influx and produced higher amounts of NO when compared with E8 cells. L-arginine (substrate for NO biosynthesis) and S-nitroso-N-acetyl-D,L-penicillamine (SNAP; a nitrosothiol NO donor) promoted extensive cell death in E6 retinas, whereas in E8 both substances decreased apoptosis. The effect of NO at both periods was mediated by soluble guanylyl cyclase (sGC) and cGMP-dependent kinase (cGK) activation. In addition, shRNA-mediated cGKII knockdown prevented NO-induced cell death (E6) and cell survival (E8). This, NO-induced cell death or cell survival was not correlated with an early inhibition of retinal cell proliferation. E6 cells also responded differentially from E8 neurons regarding cyclic AMP-responsive element-binding protein (CREB) activation in the retina in vivo. NO strongly decreased nuclear phospho-CREB staining in E6 but it robustly enhanced CREB phosphorylation in the nuclei of E8 neurons, an effect that was completely abrogated by cGKII shRNAs at both embryonic stages. The ability of NO in regulating CREB differentially during retinal development relied on the capacity of cGKII in decreasing (E6) or increasing (E8) nuclear AKT (V-Akt murine thymoma viral oncogene) activation. Accordingly, inhibiting AKT prevented both cGKII shRNA-mediated CREB upregulation in E6 and SNAP-induced CREB activation in E8. Furthermore, shRNA-mediated in vivo cGKII or in vitro CREB1 knockdown confirmed that NO/cGKII dualistically regulated the downstream CREB1 pathway and caspase activation in the chick retina to modulate neuronal viability. These data demonstrate that NO-mediated cGKII signaling may function to control the viability of neuronal cells during early retinal development via AKT/CREB1 activity.
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