Overexpression of HDAC6, but not HDAC3 and HDAC4 in the penumbra after photothrombotic stroke in the rat cerebral cortex and the neuroprotective effects of α-phenyl tropolone, HPOB, and sodium valproate

Demyanenko, Svetlana; Dzreyan, Valentina; Uzdensky, Anatoly B.

doi:10.1016/j.brainresbull.2020.06.010

Cited by 18 publications

(13 citation statements)

References 52 publications

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“…During the first two weeks after the photothrombotic stroke, HDAC6 was upregulated in the neurons not only in the penumbra, but also in the contralateral cerebral cortex, where it appeared in the neuronal nuclei. In the PTS-induced penumbra, HDAC6 co-localized with apoptotic neurons that indicated its involvement in neuronal apoptosis [57,63].…”

Section: Class II Hdacsmentioning

confidence: 98%

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Histone Deacetylases and Their Isoform-Specific Inhibitors in Ischemic Stroke

2021

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Cerebral ischemia is the second leading cause of death in the world and multimodal stroke therapy is needed. The ischemic stroke generally reduces the gene expression due to suppression of acetylation of histones H3 and H4. Histone deacetylases inhibitors have been shown to be effective in protecting the brain from ischemic damage. Histone deacetylases inhibitors induce neurogenesis and angiogenesis in damaged brain areas promoting functional recovery after cerebral ischemia. However, the role of different histone deacetylases isoforms in the survival and death of brain cells after stroke is still controversial. This review aims to analyze the data on the neuroprotective activity of nonspecific and selective histone deacetylase inhibitors in ischemic stroke.

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Section: Class II Hdacsmentioning

confidence: 98%

“…On one hand, some authors have reported the ability of HDAC4 to maintain neuronal survival [53][54][55]. However, other authors did not find a dependence of neuronal survival on HDAC4 expression [56,57]. In cultured neurons, HDAC4 rapidly translocates into the nucleus under glutamate release, or decreased K + concentration in the medium.…”

Section: Class II Hdacsmentioning

confidence: 99%

Histone Deacetylases and Their Isoform-Specific Inhibitors in Ischemic Stroke

2021

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“…Inhibition of HDAC3 or HDAC6 expression increased cell viability [ 21 ]. After PTS, HDAC6 expression was high both on the first day, and in the early recovery period [ 22 ]. Decreased HDAC6 activity caused by the selective HDAC6 inhibitors tubastatin A [ 23 ] or HPOB [ 22 ], restores acetylation of α-tubulin, a classic substrate of HDAC6, and reduces apoptosis of nerve cells, thereby protecting the brain tissue from damage.…”

Section: Histone Deacetylasesmentioning

confidence: 99%

“…Some authors reported the ability of HDAC4 to support neuronal survival [ 29 , 30 ]. Others did not find a relationship between neuronal survival and HDAC4 expression [ 22 , 31 ]. HDAC4 rapidly translocates into the nucleus in response to a decrease in potassium or an increase in glutamate in cultured neurons, which induces neuronal cell death [ 32 , 33 ].…”

Section: Histone Deacetylasesmentioning

confidence: 99%

“…Kassis et al reported that HDAC4 nuclear localization promotes brain recovery after stroke [ 34 ]. A decrease in HDAC4 expression and its translocation into neuronal nuclei was noted both on the first day, and 2 weeks after stroke [ 22 , 35 ]. It has been shown that miR-29a-3p strengthened the effect of dexmedetomidine on improving neurologic damage in newborn rats with hypoxic-ischemic brain damage by inhibiting HDAC4 [ 36 ].…”

Section: Histone Deacetylasesmentioning

confidence: 99%

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The Role of Post-Translational Acetylation and Deacetylation of Signaling Proteins and Transcription Factors after Cerebral Ischemia: Facts and Hypotheses

Demyanenko

Sharifulina

2021

IJMS

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Histone deacetylase (HDAC) and histone acetyltransferase (HAT) regulate transcription and the most important functions of cells by acetylating/deacetylating histones and non-histone proteins. These proteins are involved in cell survival and death, replication, DNA repair, the cell cycle, and cell responses to stress and aging. HDAC/HAT balance in cells affects gene expression and cell signaling. There are very few studies on the effects of stroke on non-histone protein acetylation/deacetylation in brain cells. HDAC inhibitors have been shown to be effective in protecting the brain from ischemic damage. However, the role of different HDAC isoforms in the survival and death of brain cells after stroke is still controversial. HAT/HDAC activity depends on the acetylation site and the acetylation/deacetylation of the main proteins (c-Myc, E2F1, p53, ERK1/2, Akt) considered in this review, that are involved in the regulation of cell fate decisions. Our review aims to analyze the possible role of the acetylation/deacetylation of transcription factors and signaling proteins involved in the regulation of survival and death in cerebral ischemia.

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