ArticleFrontiers in neuroscience2020
Tyro3 Contributes to Retinal Ganglion Cell Function, Survival and Dendritic Density in the Mouse Retina.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- TEAD3 + high-risk melanoma cells crosstalk with GAS6 + macrophages via the GAS6-TYRO3 ligand-receptor axis to modulate propionate metabolism and drive melanoma progression.Journal of experimental & clinical cancer research : CR · 2025Article
- Role and Mechanisms of Tyro3 in Podocyte Biology and Glomerular Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Retinal hyperspectral imaging in mouse models of Parkinson's disease and healthy aging.Scientific reports · 2024Article
- Levodopa Rescues Retinal Function in the Transgenic A53T Alpha-Synuclein Model of Parkinson's Disease.Biomedicines · 2024Article
- Tyro3 promotes the maturation of glutamatergic synapses.Frontiers in neuroscience · 2024Article
- Retinal alpha-synuclein accumulation correlates with retinal dysfunction and structural thinning in the A53T mouse model of Parkinson's disease.Frontiers in neuroscience · 2023Article
- TAM Signaling in the Nervous System.Brain plasticity (Amsterdam, Netherlands) · 2021Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal ganglion cells (RGCs) are the only output neurons of the vertebrate retina, integrating signals from other retinal neurons and transmitting information to the visual centers of the brain. The death of RGCs is a common outcome in many optic neuropathies, such as glaucoma, demyelinating optic neuritis and ischemic optic neuropathy, resulting in visual defects and blindness. There are currently no therapies in clinical use which can prevent RGC death in optic neuropathies; therefore, the identification of new targets for supporting RGC survival is crucial in the development of novel treatments for eye diseases. In this study we identify that the receptor tyrosine kinase, Tyro3, is critical for normal neuronal function in the adult mouse retina. The loss of Tyro3 results in a reduction in photoreceptor and RGC function as measured using electroretinography. The reduction in RGC function was associated with a thinner retinal nerve fiber layer and fewer RGCs. In the central retina, independent of the loss of RGCs, Tyro3 deficiency resulted in a dramatic reduction in the number of RGC dendrites in the inner plexiform layer. Our results show that Tyro3 has a novel, previously unidentified role in retinal function, RGC survival and RGC morphology. The Tyro3 pathway could therefore provide an alternative, targetable pathway for RGC protective therapeutics.
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