Synthesis of docosahexaenoic acid by retina and retinal pigment epithelium

Biochemistry ◽  
1993 ◽  
Vol 32 (49) ◽  
pp. 13703-13709 ◽  
Author(s):  
Nan Wang ◽  
Robert E. Anderson
1993 ◽  
Vol 71 (9) ◽  
pp. 690-698 ◽  
Author(s):  
Nicolas G. Bazan ◽  
Elena B. Rodriguez de Turco ◽  
William C. Gordon

Docosahexaenoic acid (22:6n−3) esterified into phospholipids represents by far the most prevalent fatty acid of rod photoreceptor disc membranes and synaptic terminals. During synaptogenesis and photoreceptor biogenesis, plasma lipoproteins, secreted mainly by the liver, are the main source of plasma 22:6n−3 for the central nervous system. This systemic route (the long loop) also operates in mature animals for morphogenesis and maintenance of excitable membranes (e.g., during constant renewal of photoreceptor disc membranes). When radiolabeled 18:3n−3, the dietary precursor of 22:6n−3, is systemically supplied to 3-day-old mouse pups, it is elongated and desaturated in the liver, leading to the synthesis of 22:6n−3 – lipoproteins that shuttle the fatty acid through the bloodstream to retina and brain. When radiolabeled 22:6n−3 was used, a more efficient labeling of brain and retinal lipids was achieved. The retinal pigment epithelium is involved, not only in the uptake of 22:6n−3 from circulating lipoproteins in the choriocapillaris but also in the recycling of 22:6n−3 from degraded phagosomal phospholipids back to the inner segments of photoreceptors (the short loop), following each phagocytic event. An interplay among efficient 22:6n−6 delivery from the liver, selective uptake by retinal pigment epithelium photoreceptor cells, and avid retinal retention may contribute to the enrichment of excitable membranes of the retina with 22:6n−3 – phospholipids.Key words: docosahexaenoic acid, phospholipids, photoreceptors.


1992 ◽  
Vol 55 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Huiming Chen ◽  
Rex D. Wiegand ◽  
Cynthia A. Koutz ◽  
Robert E. Anderson

Author(s):  
G.E. Korte ◽  
M. Marko ◽  
G. Hageman

Sodium iodate iv. damages the retinal pigment epithelium (RPE) in rabbits. Where RPE does not regenerate (e.g., 1,2) Muller glial cells (MC) forma subretinal scar that replaces RPE. The MC response was studied by HVEM in 3D computer reconstructions of serial thick sections, made using the STEREC0N program (3), and the HVEM at the NYS Dept. of Health in Albany, NY. Tissue was processed for HVEM or immunofluorescence localization of a monoclonal antibody recognizing MG microvilli (4).


Marine Drugs ◽  
2020 ◽  
Vol 19 (1) ◽  
pp. 1
Author(s):  
Peeraporn Varinthra ◽  
Shun-Ping Huang ◽  
Supin Chompoopong ◽  
Zhi-Hong Wen ◽  
Ingrid Y. Liu

Age-related macular degeneration (AMD) is a progressive eye disease that causes irreversible impairment of central vision, and effective treatment is not yet available. Extracellular accumulation of amyloid-beta (Aβ) in drusen that lie under the retinal pigment epithelium (RPE) has been reported as one of the early signs of AMD and was found in more than 60% of Alzheimer’s disease (AD) patients. Extracellular deposition of Aβ can induce the expression of inflammatory cytokines such as IL-1β, TNF-α, COX-2, and iNOS in RPE cells. Thus, finding a compound that can effectively reduce the inflammatory response may help the treatment of AMD. In this research, we investigated the anti-inflammatory effect of the coral-derived compound 4-(phenylsulfanyl) butan-2-one (4-PSB-2) on Aβ1-42 oligomer (oAβ1-42) added to the human adult retinal pigment epithelial cell line (ARPE-19). Our results demonstrated that 4-PSB-2 can decrease the elevated expressions of TNF-α, COX-2, and iNOS via NF-κB signaling in ARPE-19 cells treated with oAβ1-42 without causing any cytotoxicity or notable side effects. This study suggests that 4-PSB-2 is a promising drug candidate for attenuation of AMD.


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