Protection of injured retinal ganglion cell dendrites and unfolded protein response resolution after long-term dietary resveratrol

Lindsey, James D.; Duong-Polk, Karen X.; Hammond, Dustin; Leung, Christopher Kai-Shun; Weinreb, Robert N.

doi:10.1016/j.neurobiolaging.2014.12.021

Cited by 48 publications

(38 citation statements)

References 40 publications

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“…28,29 It has been reported that pretreatment or posttreatment with RES, primarily by oral administration, provides neuroprotection in glaucoma, but the underlying mechanisms were largely unknown. [30][31][32] Considering that many studies have shown that oral bioavailability of RES was less than 1%, which has possibly caused discrepancies between many in vitro and in vivo studies on RES, pretreatment plus posttreatment with RES has been performed in our retinal I/R injury models. 38,39 We further investigated the mechanisms underlying RES's protective effects on glaucoma.…”

Section: Discussionmentioning

confidence: 99%

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Resveratrol Delays Retinal Ganglion Cell Loss and Attenuates Gliosis-Related Inflammation From Ischemia-Reperfusion Injury

Luo

Liu

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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Section: Discussionmentioning

confidence: 99%

“…28,29 Several recent reports have shown that pretreatment or posttreatment with RES effectively protects injured RGCs in experimental glaucoma models. [30][31][32] However, the precise mechanisms by which RES protects RGCs are still largely unknown.…”

mentioning

confidence: 99%

Resveratrol Delays Retinal Ganglion Cell Loss and Attenuates Gliosis-Related Inflammation From Ischemia-Reperfusion Injury

Luo

Liu

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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“…Thy1-YFP mice have been used extensively for studying RGC morphology, physiology, development, and degeneration [31,[60][61][62][63][64][65][66][67][68]. We recently tested whether the death of YFP-expressing RGCs of these mice could represent the death of total RGCs induced by NMDA excitotoxicity.…”

Section: Yfp-expressing Rgcs Of Yfp-h Mice Are More Resistant To Onc mentioning

confidence: 99%

The Susceptibility of Retinal Ganglion Cells to Optic Nerve Injury is Type Specific

Yang

Young

Wang

et al. 2020

Cells

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Retinal ganglion cell (RGC) death occurs in many eye diseases, such as glaucoma and traumatic optic neuropathy (TON). Increasing evidence suggests that the susceptibility of RGCs varies to different diseases in an RGC type-dependent manner. We previously showed that the susceptibility of several genetically identified RGC types to N-methyl-D-aspartate (NMDA) excitotoxicity differs significantly. In this study, we characterize the susceptibility of the same RGC types to optic nerve crush (ONC). We show that the susceptibility of these RGC types to ONC varies significantly, in which BD-RGCs are the most resistant RGC type while W3-RGCs are the most sensitive cells to ONC. We also show that the survival rates of BD-RGCs and J-RGCs after ONC are significantly higher than their survival rates after NMDA excitotoxicity. These results are consistent with the conclusion that the susceptibility of RGCs to ONC varies in an RGC type-dependent manner. Further, the susceptibilities of the same types of RGCs to ONC and NMDA excitotoxicity are significantly different. These are valuable insights for understanding of the selective susceptibility of RGCs to various pathological insults and the development of a strategy to protect RGCs from death in disease conditions.

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“…The protein homeostasis (or proteostasis) is supported by a network of pathways that include: degradation - the ubiquitin proteasome and the ER–associated degradation systems; posttranslational modification -phosphorylation, acylation, and oxidation; and protein synthesis/folding/unfolding - ribosomes, the unfolded protein response (UPR) and HSF1 (Roth and Balch, 2011; Li et al, 2013; Díaz-Villanueva JF, Díaz-Molina, 2015). ER stress appears to be a common neuronal response to axonal injury: ER stress and activation of UPR has been implicated in RGC degeneration caused by ONT (Pernet et al, 2012), ONC (Hu et al, 2012; Jiang et al, 2013; Yasuda et al, 2014; Lindsey et al, 2015) and OH (Doh et al, 2010; Shimazawa et al, 2007). HSF1, as one of the important sensors of proteotoxic stress, plays a critical role in the heat shock response network that regulates the expression of molecular chaperones, such as HSPs, as well as proteinases and other inducible genes for protection and recovery from diverse forms of environmental and physiological stress.…”

Section: Hsp27 and Hsp60 In Rgc Survival Regeneration And Autoimmmentioning

confidence: 99%

Heat shock proteins in the retina: Focus on HSP70 and alpha crystallins in ganglion cell survival

Piri

Kwong

et al. 2016

Progress in Retinal and Eye Research

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Heat shock proteins (HSPs) belong to a superfamily of stress proteins that are critical constituents of a complex defense mechanism that enhances cell survival under adverse environmental conditions. Cell protective roles of HSPs are related to their chaperone functions, antiapoptotic and antinecrotic effects. HSPs' antiapoptotic and cytoprotective characteristics, their ability to protect cells from a variety of stressful stimuli, and the possibility of their pharmacological induction in cells under pathological stress make these proteins an attractive therapeutic target for various neurodegenerative diseases; these include Alzheimer's, Parkinson's, Huntington's, prion disease, and others. This review discusses the possible roles of HSPs, particularly HSP70 and small HSPs (alpha A and alpha B crystallins) in enhancing the survival of retinal ganglion cells (RGCs) in optic neuropathies such as glaucoma, which is characterized by progressive loss of vision caused by degeneration of RGCs and their axons in the optic nerve. Studies in animal models of RGC degeneration induced by ocular hypertension, optic nerve crush and axotomy show that upregulation of HSP70 expression by hyperthermia, zinc, geranyl-geranyl acetone, 17-AAG (a HSP90 inhibitor), or through transfection of retinal cells with AAV2-HSP70 effectively supports the survival of injured RGCs. RGCs survival was also stimulated by overexpression of alpha A and alpha B crystallins. These findings provide support for translating the HSP70- and alpha crystallin-based cell survival strategy into therapy to protect and rescue injured RGCs from degeneration associated with glaucomatous and other optic neuropathies.

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Protection of injured retinal ganglion cell dendrites and unfolded protein response resolution after long-term dietary resveratrol

Cited by 48 publications

References 40 publications

Resveratrol Delays Retinal Ganglion Cell Loss and Attenuates Gliosis-Related Inflammation From Ischemia-Reperfusion Injury

Resveratrol Delays Retinal Ganglion Cell Loss and Attenuates Gliosis-Related Inflammation From Ischemia-Reperfusion Injury

The Susceptibility of Retinal Ganglion Cells to Optic Nerve Injury is Type Specific

Heat shock proteins in the retina: Focus on HSP70 and alpha crystallins in ganglion cell survival

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