ER stress in retinal degeneration: a target for rational therapy?

Griciuc, Ana; Aron, Liviu; Ueffing, Marius

doi:10.1016/j.molmed.2011.04.002

Cited by 57 publications

(62 citation statements)

References 68 publications

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“…Constitutive Phototransduction Activates Endoplasmic Reticulum (ER) Stress-Overload of the UPS is known to cause ER stress and induce the UPR and vice versa (36). To examine this possibility, markers corresponding to three major arms of the UPR were analyzed by Western blots.…”

Section: Matically To the Detergent-insoluble Fraction (P) In The Arr1mentioning

confidence: 99%

“…When the UPR failed to restore homeostasis, apoptosis ensued. In addition to constitutive G-protein signaling, there are naturally occurring rhodopsin mutations in human patients afflicted with autosomal dominant retinitis pigmentosa that have a tendency to misfold, and it has been demonstrated that these mutants also induce the UPR (32,36,54). Therefore, strategies to control ER stress, either by overexpression of GRP78 (55) or application of small molecules that modulate UPR (41,56,57), may be effective in the treatment of these types of retinal degenerative diseases.…”

Section: Our Findings On Arr1mentioning

confidence: 99%

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Induction of the Unfolded Protein Response by Constitutive G-protein Signaling in Rod Photoreceptor Cells

Chen

2014

Journal of Biological Chemistry

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Background: Excessive light exposure and genetic mutations that act as "equivalent light" cause photoreceptor cell death. Results: Prolonged transducin signaling, but not channel closure, induces endoplasmic reticulum stress. Conclusion: Induction of UPR is a distinct cell death pathway caused by transducin signaling. Significance: Manipulation of UPR may prolong photoreceptor cell survival in transducin-induced retinal light damage.

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Section: Matically To the Detergent-insoluble Fraction (P) In The Arr1mentioning

confidence: 99%

Section: Our Findings On Arr1mentioning

confidence: 99%

Induction of the Unfolded Protein Response by Constitutive G-protein Signaling in Rod Photoreceptor Cells

Chen

2014

Journal of Biological Chemistry

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“…Progressively slow neurodegenerative diseases, originating from a blast induced insult, are known for the brain, such as chronic traumatic encephalopathy (CTE) (Goldstein, 2012). Histopathology of the retina and brain visual processing centers at far time points post-blast could look for "classic" biomarker proteins of chronic neuro-degeneration, such as p-tau, β-amyloid, and GFAP (Hoshino, 1998;Cao, 2001;Liberto, 2004;Griciuc, 2011).…”

Section: Resultsmentioning

confidence: 99%

Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Overpressure on Eye and Brain Visual Processing Centers in Rats

DeMar¹,

Hill²,

Gharavi³

et al. 2013

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. 5f. WORK UNIT NUMBER PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERThe Geneva Foundation Tacoma, WA 98402 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited 13. SUPPLEMENTARY NOTES None ABSTRACTUsing an adult rat model of blast wave exposure, we rigorously characterized the cellular and functional damage to the eyes (retinas) and brain visual processing centers, by electroretinography (ERG), visual discrimination behavioral testing, and histopathology. Blast wave injury was carried out by placing the rats in a compressed air driven shock tube and exposing them, in a right side on orientation, once to a 20 psi (260 Hz) blast over pressure wave. Rats were assessed at baseline and then 1, 7, and 14 days post-exposure. By 7 to 14 days out, blasted rats versus shams showed significantly decreased ERG waveform amplitudes for the right side eyes (~ 30% less; n = 15 vs.14), a trend for impaired ability to visually discern a cue light to earn food rewards (~ 30% less; n = 10 vs. 11), and significant neuronal cell degeneration within the right side retinas and both brain optic tracts (2 and 3-fold more, respectively; n = 11 vs. 11). ERG and histopathology results significantly correlated with each other (r = -0.7). There also was a strong relationship between the retina and brain optic tract cell damage (r = 0.8). Overall, our findings demonstrate that blast wave exposure leads to loss of vision in rats, likely through retinal cell death followed by anterograde degeneration of brain visual processing centers from lack of signaling input.

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“…The ER stress pathway was first identified as a cellular response that is induced by the accumulation of unfolded proteins in the ER to preserve the organelle's function. Previous studies have demonstrated that ER stress is one of the main events in the pathogenesis of MI/R injury [37][38][39][40] . Activation of the UPR in mammalians is mediated by three distinct ER stress sensors, namely, ER kinase (PERK), transcription factor ATF6, and endoribonuclease IRE-1.…”

Section: Discussionmentioning

confidence: 99%

2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress

Zhang

Zhao

et al. 2017

Acta Pharmacol Sin

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ER stress in retinal degeneration: a target for rational therapy?

Cited by 57 publications

References 68 publications

Induction of the Unfolded Protein Response by Constitutive G-protein Signaling in Rod Photoreceptor Cells

Induction of the Unfolded Protein Response by Constitutive G-protein Signaling in Rod Photoreceptor Cells

Evaluation of Novel Polyunsaturated Fatty Acid Derived Lipid Mediators of Inflammation to Ameliorate the Deleterious Effects of Blast Overpressure on Eye and Brain Visual Processing Centers in Rats

2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside protects murine hearts against ischemia/reperfusion injury by activating Notch1/Hes1 signaling and attenuating endoplasmic reticulum stress

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