Adiponectin receptor 1 conserves docosahexaenoic acid and promotes photoreceptor cell survival
Open accessAbstract
The identification of pathways necessary for photoreceptor and retinal pigment epithelium (RPE) function is critical to uncover therapies for blindness. Here we report the discovery of adiponectin receptor 1 (AdipoR1) as a regulator of these cells' functions. Docosahexaenoic acid (DHA) is avidly retained in photoreceptors, while mechanisms controlling DHA uptake and retention are unknown. Thus, we demonstrate that AdipoR1 ablation results in DHA reduction. In situ hybridization reveals photoreceptor and RPE cell AdipoR1 expression, blunted in AdipoR1(-/-) mice. We also find decreased photoreceptor-specific phosphatidylcholine containing very long-chain polyunsaturated fatty acids and severely attenuated electroretinograms. These changes precede progressive photoreceptor degeneration in AdipoR1(-/-) mice. RPE-rich eyecup cultures from AdipoR1(-/-) reveal impaired DHA uptake. AdipoR1 overexpression in RPE cells enhances DHA uptake, whereas AdipoR1 silencing has the opposite effect. These results establish AdipoR1 as a regulatory switch of DHA uptake, retention, conservation and elongation in photoreceptors and RPE, thus preserving photoreceptor cell integrity.
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AdipoR1 has an additional function independent of its cognate ligand adiponectin: it is a key regulator of DHA uptake/retention in the retina, where it is critical to maintain normal structure and function.
“We found that AdipoR1 has an additional function independent of its cognate ligand adiponectin: it is a key regulator of DHA uptake/retention in the retina (Rice et al., 2015), where it is critical to maintain the normal structure and function.”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Rice et al., 2015
Upon ablation of AdipoR1, DHA uptake is impaired and PRC-specific VLC-PUFA-containing PC molecular species are reduced, and PRC function and survival are compromised.
“Upon ablation of this receptor, DHA uptake is impaired and PRC-specific very-long-chain polyunsaturated fatty acids (VLC-PUFA)-containing PC molecular species are reduced; and PRC function and survival are compromised (Rice et al., 2015).”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Rice et al., 2015
The genetic ablation of AdipoR1 leads to depletion of the PCMS that contains C32:6n3 or C34:6n3, and DHA, which in turn leads to photoreceptor degeneration that resembles various human forms of retinal degenerative diseases.
“The genetic ablation of AdipoR1 leads to depletion of the PCMS that contains C32:6n3 or C34:6n3, and DHA (C22:6n3), which in turn leads to photoreceptor degeneration that resembles various human forms of retinal degenerative diseases (Rice et al., 2015).”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Rice et al., 2015
AdipoR1 is necessary for DHA availability to PRCs.
“Recently, we found that AdipoR1 is necessary for DHA availability to PRCs (Rice et al., 2015)”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Rice et al., 2015
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- Authors
- Rice, D. S., Calandria, J. M., Gordon, W. C., Jun, B., Zhou, Y., Gelfman, C. M., Li, S., Jin, M., Knott, E. J., Chang, B., Abuin, A., Issa, T., Potter, D., Platt, K. A., & Bazan, N. G.
- Affiliations
- Lexicon Pharmaceuticals (United States) (US)
- Louisiana State University (US)
- Jackson Laboratory (US)
- Corresponding author
- Bazan, Nicolas G.
- ORCID
- Venue
- Nature Communications
- Published
- 2015-03-04
- Volume
- 6
- Issue
- 1
- Pages
- 6228-6228
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4351799
- OpenAlex
- W1967528858
- Cited by
- 124
- References
- 49
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 13 · 2023: 11 · 2022: 15 · 2021: 12 · 2020: 9 · 2019: 8 · 2018: 10 · 2017: 13 · 2016: 11 · 2015: 7
- FWCI
- 5.93
- Type
- journal article
- Language
- en
- Update notices
- correction (2015-05-12)
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion, cc-by)
- The Novartis Repository (Novartis) (submittedVersion)
- Funders
- Research to Prevent Blindness
- National Institutes of Health (EY0-05121, 5r01ey019943-13, GM-103340)
- National Eye Institute (R01-EY019943, R01EY021208, R01EY005121)
- National Institute of General Medical Sciences (GM-103340, P30GM103340)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Keywords
- AdipoR1, docosahexaenoic acid, retinal pigment epithelium, polyunsaturated fatty acids, phosphatidylcholine, photoreceptor degeneration, electroretinogram, fatty acid elongation
- MeSH terms
- Animals, Docosahexaenoic Acids, Electroretinography, Phosphatidylcholines, In Situ Hybridization, Mice, Knockout, Photoreceptor Cells, Vertebrate, Mice, Receptors, Adiponectin, Retinal Pigment Epithelium
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