Valproic acid-mediated neuroprotection in retinal ischemia injury via histone deacetylase inhibition and transcriptional activation

Zhang, Zhenzhen; Qin, Xiuhong; Tong, Nianting; Zhao, Xinfeng; Gong, Yuanyuan; Shi, Yuhua; Wu, Xiang

doi:10.1016/j.exer.2011.11.013

Cited by 50 publications

(43 citation statements)

References 46 publications

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“…For example, we previously reported that VPA upregulates Müller glial brain-derived neurotrophic factor (BDNF) and nerve growth factor, neurotrophic factors important for cell survival [12,13,20] and these effects may also apply to the VPA-treated GLAST KO mouse retina. Also, VPA is an effective HDAC inhibitor [8,30] and increased histone acetylation is associated with VPA-mediated neuroprotection [1,3,35,40,43]. These findings urge to identify genes and pathways that are modulated by HDAC inhibition and are involved in VPA-mediated RGC protection.…”

Section: Discussionmentioning

confidence: 90%

Valproic acid prevents retinal degeneration in a murine model of normal tension glaucoma

Kimura

Guo

Noro

et al. 2015

Neuroscience Letters

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Section: Discussionmentioning

confidence: 90%

Valproic acid prevents retinal degeneration in a murine model of normal tension glaucoma

Kimura

Guo

Noro

et al. 2015

Neuroscience Letters

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“…At 1 and 2 w after ONC, retinal tissues (n = 6 each group) were harvested, The densities of the FG-positive RGCs were determined in a blind fashion using fluorescence microscopy (Zeiss 510, Jena, Germany) as previously described (Zhang et al, 2011a).…”

Section: Retrograde Labeling Of Retinal Ganglion Cells With Fluorogolmentioning

confidence: 99%

“…Our previous studies show that VPA provides neuroprotection of the retina and reduces optic nerve axonal damage induced by retinal ischemia/reperfusion (Zhang et al, 2011a;Zhang et al, 2011b;Zhang et al, 2012). In addition, the suppression of HDAC activity can protect the retina from ischemic injury (Crosson et al, 2010).…”

Section: Introductionmentioning

confidence: 98%

Valproate promotes survival of retinal ganglion cells in a rat model of optic nerve crush

et al. 2012

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“…The epigenetic influence of HDIs on gene expression make them a useful new class of pharmacological agents that could ameliorate various disease conditions. For example, HDIs also promote neuronal survival in ischemic injury, [14][15][16][17] multiple sclerosis [18,19], and Alzheimer's and Huntington's disease models [20][21][22][23][24]. These multiple roles of HDIs can be attributed to alterations in the expression of different gene sets by increasing acetylation of chromatin.…”

Section: Introductionmentioning

confidence: 99%

Scriptaid, a Novel Histone Deacetylase Inhibitor, Protects Against Traumatic Brain Injury via Modulation of PTEN and AKT Pathway

Wang

Jiang

et al. 2013

Neurotherapeutics

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Traumatic brain injury (TBI) is a leading cause of motor and cognitive deficits in young adults for which there is no effective therapy. The present study characterizes the protective effect of a new histone deacetylase inhibitor, Scriptaid (SigmaAldrich Corporation, St. Louis, MO), against injury from controlled cortical impact (CCI). Scriptaid elicited a dose-dependent decrease in lesion size at 1.5 to 5.5 mg/kg and a concomitant attenuation in motor and cognitive deficits when delivered 30 minutes postinjury in a model of moderate TBI. Comparable protection was achieved even when treatment was delayed to 12 h postinjury. Furthermore, the protection of motor and cognitive functions was long lasting, as similar improvements were detected 35 days postinjury. The efficacy of Scriptaid (SigmaAldrich Corporation) was manifested as an increase in surviving neurons, as well as the number/length of their processes within the CA3 region of the hippocampus and the pericontusional cortex. Consistent with other histone deacetylase inhibitors, Scriptaid treatment prevented the decrease in phospho-AKT (p-AKT) and phosphorylated phosphatase and tensin homolog deleted on chromosome 10 (p-PTEN) induced by TBI in cortical and CA3 hippocampal neurons. Notably, the p-AKT inhibitor LY294002 attenuated the impact of Scriptaid, providing mechanistic evidence that Scriptaid functions partly by modulating the prosurvival AKT signaling pathway. As Scriptaid offers longlasting neuronal and behavioral protection, even when delivered 12 h after controlled cortical impact, it is an excellent new candidate for the effective clinical treatment of TBI.

show abstract

Valproic acid-mediated neuroprotection in retinal ischemia injury via histone deacetylase inhibition and transcriptional activation

Cited by 50 publications

References 46 publications

Valproic acid prevents retinal degeneration in a murine model of normal tension glaucoma

Valproic acid prevents retinal degeneration in a murine model of normal tension glaucoma

Valproate promotes survival of retinal ganglion cells in a rat model of optic nerve crush

Scriptaid, a Novel Histone Deacetylase Inhibitor, Protects Against Traumatic Brain Injury via Modulation of PTEN and AKT Pathway

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