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Printable Handouts
Navigable Slide Index
- Introduction
- AdipoR1 is an integral membrane protein
- AdipoR1 polymorphism references
- Biosynthesis of docosanoids: neuroprotectin D1
- Stereoselective lipid mediator neuroprotectin D1
- Photoreceptor outer segment phagocytosis attenuates oxidative stress-induced apoptosis
- A2E accumulates in the RPE in Stargardt’s syndrome and in age-related macular degeneration
- Neurotrophins regulate NPD1 synthesis
- Inducers of NPD1 synthesis and bioactivity in the RPE cell
- Eicosanoids and docosanoids in neuroinflammation
- NPD1 induces protective microglia to modulate neuroinflammatory signalling
- Age-related macular degeneration
- Changes in microglia and astroglia in Alzheimer’s disease
- Onset and progression of AMD
- NPD1 attenuates choroid neovascularization
- Microglia distribution
- NPD1 induces protective _x000B_microglia phenotypes
- NPD1 modulates inflammatory transcription to confront homeostatic disruptions in the RPE cell
- cIAP2 /BIRC3 expression is induced by NPD1
- NPD1 sterospecifically upregulates “de novo” transcription of BIRC3
- BIRC3 selectively up-regulated by NPD1
- NPD1 enhances the activation of BIRC3 promoter
- Transcriptional regulation of c-REL by NPD1 in the RPE cell
- Up-regulation of BIRC3 transcription by NPD1-dependent c-REL expression
- NPD1 inhibits apoptosis during uncompensated oxidative stress
- Biosynthesis of elovanoids
- Phosphatidyl choline molecular species with VLC-PUFA (n-3) are reduced in adipoR1 KO
- PC molecular species in 24-day-old mouse retinas
- Photoreceptor cells and neurons selectively express ELOVL4
- ELOVL4 (ELOngation of Very Long chain fatty acids-4)
- ELOVL4 is not down-regulated in adipoR1–/– retinas
- Primary human RPE cells
- Elovanoids 32 and 34
- Elovanoids enhance abundance of pro-homeostatic proteins
- Elovanoids decrease abundance of proteins engaged in cell damage and apoptosis
- Light activates release of 32:6n-3, 34:6n-3 and formation of ELV precursors
- STGD3 ELOVL4 mutation
- Intercellular cooperation for elovanoids synthesis and bioactivity
- Long loop for supply and short-loop for conservation/retention of DHA in PRC
- Relationship between photoreceptor cells and retinal pigment epithelial cells
- DHA is supplied by the long loop and retained by short loop
- Spatial organization of lipids in the human retina and optic nerve by MALDI
- Conclusions (1)
- Neuroprotectin D1
- Conclusions (2)
- Elovanoids
- Acknowledgements
Topics Covered
- AdipoR1 as an integral membrane protein
- Neuroprotectin D1
- Eicosanoids and docosanoids in neuroinflammation
- Biosynthesis of elovanoids and expression of ELOVL4
- Relationship between photoreceptor cells and retinal pigment epithelial cells
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Talk Citation
Bazan, N. (2019, September 26). Photoreceptor protection: significance of docosanoids and elovanoids 2: bioactive derivatives of DHA [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 23, 2024, from https://doi.org/10.69645/LDWR7506.Export Citation (RIS)
Publication History
Financial Disclosures
- N. Bazan is the named inventor of technologies, models and compositional matter related to this presentation. Intellectual Property are assigned to Louisiana State University Health, New Orleans, Louisiana, USA and to Neuresto Therapeutics, LLC.
Photoreceptor protection: significance of docosanoids and elovanoids 2: bioactive derivatives of DHA
Published on September 26, 2019
40 min
Other Talks in the Series: Macular Degeneration
Transcript
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0:00
This is Nicolas G. Bazan from
LSU Neuroscience Center of Excellence at
Louisiana State University School of Medicine in New Orleans.
I would like, in the second part,
to introduce bioactive derivatives of docosahexaenoic acid.
0:16
It's a little farther synthesis of what I have shown you up to now in the context, again,
of the importance of adiponectin reciprocal 1 as
an integral membrane protein necessary
for the maintenance of photoreceptor cell structure and function
because of the ablation of adiponectin recipient 1 leads to number 1,
flecked retina and photoreceptor cell degeneration; secondly,
attenuated electroretinogram and prolonged dark recovery;
thirdly, impaired retinal visual cycle; fourth,
adiponectin knockout- the cognate ligand does not display retinal degeneration phenotype.
It is very interesting that after
the paper that reported on the adiponectin receptor knockout,
many other studies began pointing out too, for example,
mutations of a single amino acid in
the adiponectin receptor 1 that lead to retinitis pigmentosa.
In fact, they may explain as many as 40-45 percent of the cases of retinitis pigmentosa.
Previous studies have suggested that certain Finnish populations that have
age-related macular degeneration display polymorphisms
in adiponectin receptor 1 assume variance.
1:39
That is actually in the next slide,
the top one is a paper that refers to a mutation in the AdipoR1
as causing nonsyndromic autosomal dominant retinitis pigmentosa.
The second reference there is the AdipoR1 mutated in,
again, retinitis pigmentosa from another group.
The bottom one is actually the body and associated with
advance age-related macular degeneration in a Finnish population.
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