Expression of Histone Deacetylases HDAC1 and HDAC2 and Their Role in Apoptosis in the Penumbra Induced by Photothrombotic Stroke

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

doi:10.1007/s12035-019-01772-w

Cited by 21 publications

(16 citation statements)

References 37 publications

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“…Currently, a study has implied an increment in the expression of HDAC1 in depressive-like and anxiety-like phenotypes resulted by stress-offspring [21]. Moreover, the expression of HDAC1 is documented to up-regulate in penumbra in photothrombotic stroke [22]. Besides that, the incremental HDAC1 mRNA expression is found in granule and pyramidal cells in temporal lobe epilepsy [23].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: HDAC1-Mediated MicroRNA-124-5p Regulates NPY to Affect Learning and Memory Abilities in Rats with Depression

Tang

2021

Nanoscale Res Lett

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Researches pivoting on histone deacetylases (HDACs) in depression have been excessively conducted, but not much on HDAC1. Therein, the present study is launched to disclose the mechanism of HDAC1/microRNA (miR)-124-5p/neuropeptide Y (NPY) axis in depression. Sprague Dawley rats were stimulated by chronic unpredictable mild stress to establish depression models. Depressed rats were injected with inhibited HDAC1 or suppressed miR-124-5p to explore their roles in body weight, learning and memory abilities, oxidative stress and inflammation in serum and neurotransmitter expression in hippocampal tissues. MiR-124-5p, HDAC1 and NPY expression in the hippocampus were tested. The interactions of miR-124-5p, HDAC1 and NPY expression were also confirmed. Higher miR-124-5p and HDAC1 and lower NPY expression levels were found in the hippocampus of depressed rats. Inhibited miR-124-5p or suppressed HDAC1 attenuated learning and memory abilities and increased body weight of depressed rats. Knockdown of miR-124-5p or inhibition of HDAC1 suppressed oxidative stress and inflammation and promoted neurotransmitter expression of depressed rats. HDAC1 mediated miR-124-5p to regulate NPY. Knockdown of NPY abolished the protective effects of inhibited miR-124-5p on depressed rats. Our study illustrates that suppression of either miR-124-5p or HDAC1 up-regulates NPY to improve memory and learning abilities in depressed mice, which may update the existed knowledge of depression and provide a novel reference for treatment of depression.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: HDAC1-Mediated MicroRNA-124-5p Regulates NPY to Affect Learning and Memory Abilities in Rats with Depression

Tang

2021

Nanoscale Res Lett

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“…PTS increases the expression of HDAC1 and HDAC2 in the penumbra, which leads to the redistribution of HDAC1. However, the redistribution of HDAC2 from the nucleus to the cytoplasm is less than that of HDAC1 [ 28 ]. In transient middle cerebral artery occlusion (tMCAO) models of rats, the specificity protein family of transcription factor 3 (Sp3) together with HDAC1/HDAC2 complex could modulate the acetylation of ncx1 brain promoter (ncx1-br), which may act as an innovative development strategy in stroke treatment intervention [ 29 ].…”

Section: Hdacs In Cerebral Ischemiamentioning

confidence: 99%

Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke

Wang

Chen

et al. 2020

Disease Markers

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Background. Cerebral ischemic stroke is one of the severe diseases with a pathological condition that leads to nerve cell dysfunction with seldom available therapy options. Currently, there are few proven effective treatments available for improving cerebral ischemic stroke outcome. However, recently, there is increasing evidence that inhibition of histone deacetylase (HDAC) activity exerts a strong protective effect in in vivo and vitro models of ischemic stroke. Review Summary. HDAC is a posttranslational modification that is negatively regulated by histone acetyltransferase (HATS) and histone deacetylase. Based on function and DNA sequence similarity, histone deacetylases (HDACs) are organized into four different subclasses (I-IV). Modifications of histones play a crucial role in cerebral ischemic affair development after translation by modulating disrupted acetylation homeostasis. HDAC inhibitors (HDACi) mainly exert neuroprotective effects by enhancing histone and nonhistone acetylation levels and enhancing gene expression and protein modification functions. This article reviews HDAC and its inhibitors, hoping to find meaningful therapeutic targets. Conclusions. HDAC may be a new biological target for cerebral ischemic stroke. Future drug development targeting HDAC may make it a potentially effective anticerebral ischemic stroke drug.

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“…Quantitative assessment of fluorescence of experimental and control preparations was carried out using 10-15 images acquired with the same camera settings as described previously (Demyanenko et al, 2020). Briefly, the corrected total cell fluorescence (CTCF) was calculated for The co-localization of sirtuins with synaptophysin, GAP43, acetylated α-tubulin, the neuron markers (NSE or NeuN), the astrocytes marker (GFAP) and the nuclear marker Hoecsht33342 (10 μg/ml; blue signal) was evaluated using the Image J program (http://rsb.info.nih.gov/ij/) with the JACoP plugin (Bolte and Cordelières, 2006).…”

Section: Immunofluorescence Staining and Image Analysismentioning

confidence: 99%

Localization and Expression of Sirtuins 1, 2, 6 and Plasticity-Related Proteins in the Recovery Period after a Photothrombotic Stroke in Mice

Demyanenko

Gantsgorn

Rodkin

et al. 2020

Journal of Stroke and Cerebrovascular Diseases

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Sirtuins, class III histone deacetylases, are involved in the regulation of tissue repair processes and brain functions after a stroke. The ability of some isoforms of sirtuins to circulate between the nucleus and cytoplasm may have various pathophysiological effects on the cells. In present work, we focused on the role of non-mitochondrial sirtuins SIRT1, SIRT2, and SIRT6 in the restoration of brain cells following ischemic stroke. Here, using a photothrombotic stroke (PTS) model in mice, we studied whether local stroke affects the level and intracellular localization of SIRT1, SIRT2, and SIRT6 in neurons and astrocytes of the intact cerebral cortex adjacent to the ischemic ipsilateral hemisphere and in the analogous region of the contralateral hemisphere at different time points during the recovery period after a stroke. We evaluated the co-localization of sirtuins with growth-associated protein-43 (GAP-43), the presynaptic marker synaptophysin (SYN) and acetylated α-tubulin (Ac-α-Tub), that are associated with brain plasticity and are known to be involved in brain repair after a stroke. The results show that during the recovery period, an increase in SIRT1 and SIRT2 levels occurred. The increase of SIRT1 level was associated with an increase in synaptic plasticity proteins, whereas the increase of SIRT2 level was associated with an acetylated of α-tubulin, that can reduce the mobility of neurites. SIRT6 co-localized with GAP-43, but not with SYN. Moreover, we showed that SIRT1, SIRT2, and SIRT6 are not involved in the PTS-induced apoptosis of penumbra cells. Taken together, our results suggest that sirtuins functions differ depending on cell type, intracellular localization, specificity of sirtuins isoforms to different substrates and nature of post-translational modifications of enzymes.

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Expression of Histone Deacetylases HDAC1 and HDAC2 and Their Role in Apoptosis in the Penumbra Induced by Photothrombotic Stroke

Cited by 21 publications

References 37 publications

RETRACTED ARTICLE: HDAC1-Mediated MicroRNA-124-5p Regulates NPY to Affect Learning and Memory Abilities in Rats with Depression

RETRACTED ARTICLE: HDAC1-Mediated MicroRNA-124-5p Regulates NPY to Affect Learning and Memory Abilities in Rats with Depression

Updating a Strategy for Histone Deacetylases and Its Inhibitors in the Potential Treatment of Cerebral Ischemic Stroke

Localization and Expression of Sirtuins 1, 2, 6 and Plasticity-Related Proteins in the Recovery Period after a Photothrombotic Stroke in Mice

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