ArticleJournal of molecular neuroscience : MN2015
Raf-1 Kinase Inhibitory Protein (RKIP) Promotes Retinal Ganglion Cell Survival and Axonal Regeneration Following Optic Nerve Crush.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- PEBP1 Regulates Ferroptosis in Acute Glaucoma: Targeted Therapy Using Engineered Exosomes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Rare variant analyses across multiethnic cohorts identify novel genes for refractive error.Communications biology · 2023Article
- Axonal degeneration induces distinct patterns of phosphatidylserine and phosphatidylethanolamine externalization.Cell death discovery · 2021Article
- PEBP1/RKIP behavior: a mirror of actin-membrane organization.Cellular and molecular life sciences : CMLS · 2020Article
- Strategies to Promote Long-Distance Optic Nerve Regeneration.Frontiers in cellular neuroscience · 2020Article
- MEK inhibition prevents TGF‑β1‑induced myofibroblast transdifferentiation in human tenon fibroblasts.Molecular medicine reports · 2019Article
- Metabolomic changes in the mouse retina after optic nerve injury.Scientific reports · 2018Article
- Specific Phospholipids Regulate the Acquisition of Neuronal and Astroglial Identities in Post-Mitotic Cells.Scientific reports · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Raf-1 kinase inhibitory protein (RKIP), a member of the phosphatidylethanolamine-binding protein (PEBP) family, plays an important role in neuronal apoptosis and cognitive deficits associated with neurodegenerative diseases. However, the biological function of RKIP in the retina is still unclear. Therefore, in the present study, we investigated the expression of RKIP in mouse retina following optic nerve crush (ONC) and evaluated the effects of RKIP on retinal ganglion cells (RGCs) apoptosis and axonal regeneration after ONC. Our results showed that the expression of RKIP was markedly decreased in the injured retina. Overexpression of RKIP inhibits RGC apoptosis and promotes axonal regeneration after ONC. Furthermore, overexpression of RKIP significantly increased the phosphorylation in extracellular signal-related kinase (ERK)1/2 and AKT in the injured retina. Taken together, these results suggest that RKIP promotes RGCs survival and axonal regeneration following ONC through promoting the ERK signaling pathway, implying that RKIP may serve as a potential molecular target for the treatment of glaucoma.
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Registered trials
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