Fatty Acid Transport Protein 4 (FATP4) Prevents Light-Induced Degeneration of Cone and Rod Photoreceptors by Inhibiting RPE65 Isomerase
Open accessAbstract
Although rhodopsin is essential for sensing light for vision, it also mediates light-induced apoptosis of photoreceptors in mouse. RPE65, which catalyzes isomerization of all-trans retinyl fatty acid esters to 11-cis-retinol (11 c ROL) in the visual cycle, controls the rhodopsin regeneration rate and photoreceptor susceptibility to light-induced degeneration. Mutations in RPE65 have been linked to blindness in affected children. Despite such importance, the mechanism that regulates RPE65 function remains unclear. Through unbiased expression screening of a bovine retinal pigment epithelium (RPE) cDNA library, we have identified elongation of very long-chain fatty acids-like 1 (ELOVL1) and fatty acid transport protein 4 (FATP4), which each have very long-chain fatty acid acyl-CoA synthetase (VLCFA-ACS) activity, as negative regulators of RPE65. We found that the VLCFA derivative lignoceroyl (C24:0)-CoA inhibited synthesis of 11 c ROL, whereas palmitoyl (C16:0)-CoA promoted synthesis of 11 c ROL. We further found that competition of FATP4 with RPE65 for the substrate of RPE65 was also involved in the mechanisms by which FATP4 inhibits synthesis of 11 c ROL. FATP4 was predominantly expressed in RPE, and the FATP4-deficient RPE showed significantly higher isomerase activity. Consistent with these results, the regeneration rate of 11-cis-retinaldehyde and the recovery rate for rod light sensitivity were faster in FATP4-deficient mice than wild-type mice. Moreover, FATP4-deficient mice displayed increased accumulation of the cytotoxic all-trans retinaldehyde and hypersusceptibility to light-induced photoreceptor degeneration. Our findings demonstrate that ELOVL1, FATP4, and their products comprise the regulatory elements of RPE65 and play important roles in protecting photoreceptors from degeneration induced by light damage.
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Retinoic acid has been suggested to participate in the downregulation of RPE65 and of FATP4 and ELOVL1.
“Retinoic acid has been suggested to participate in the downregulation of RPE65 ( 40 ) and of fatty acid transporter protein 4 (FATP4) and elongation of very-long-chain fatty acid protein 1 (ELOVL1) ( 41 ).”
From Loss of Extracellular Signal-Regulated Kinase 1/2 in the Retinal Pigment Epithelium Leads to RPE65 Decrease and Retinal Degeneration (2017) · cites this paper as [41]
Citation 41 is attached to the proposed downregulation of FATP4 and ELOVL1 by retinoic acid. The Discussion reports that FATP4 and ELOVL1 inhibit RPE65-catalyzed isomerization, but neither it nor the passages retrieved for retinoic-acid regulation address whether retinoic acid downregulates either protein. Our copy provides no page number for these passages. (LLM, conf=0.76)
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- Authors
- Li, S., Lee, J., Zhou, Y., Gordon, W. C., Hill, J. M., Bazan, N. G., Miner, J. H., & Jin, M.
- Affiliations
- Louisiana State University Health Sciences Center New Orleans (US)
- Cellerant Therapeutics (United States) (US)
- Washington University in St. Louis (US)
- Corresponding author
- Jin, Minghao
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2013-02-13
- Volume
- 33
- Issue
- 7
- Pages
- 3178-3189
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3625017
- OpenAlex
- W1990589135
- Cited by
- 36
- References
- 52
- Citations by year
- 2026: 3 · 2024: 4 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 4 · 2019: 1 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 4 · 2014: 2 · 2013: 3
- FWCI
- 1.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
- Funders
- Louisiana State University
- National Institutes of Health
- National Eye Institute (R01EY021208, EY021208)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR049269, AR049269)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- FATP4, RPE65, ELOVL1, visual cycle, very long chain fatty acids, retinal pigment epithelium, photoreceptor degeneration, rhodopsin regeneration, rod and cone photoreceptors
- MeSH terms
- Fatty Acid Elongases, Retinoid Isomerohydrolase, Acetyltransferases, Alcohol Oxidoreductases, Animals, Cells, Cultured, Electroretinography, Gene Expression Regulation, Immunohistochemistry, Light, Mice, Inbred C57BL, Peptide Chain Elongation, Translational, Phenotype, Retinal Degeneration, Retinoids, Transfection, Blotting, Western, Gene Library, Retinal Rod Photoreceptor Cells, Retinal Cone Photoreceptor Cells, Mice, Knockout, cis-trans-Isomerases, Fatty Acid Transport Proteins, Mice, Real-Time Polymerase Chain Reaction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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