Selective regulation of class I and class II histone deacetylases expression by inhibitors of histone deacetylases in cultured mouse neural cells

Ajamian, Farzam; Salminen, Antero; Reeben, Mati

doi:10.1016/j.neulet.2004.04.087

Cited by 39 publications

(31 citation statements)

References 19 publications

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“…KDAC-dependent regulation of basal and cytokine-induced expression of Hdac1, Hdac2, Hdac6 and Hdac11 mRNA In non-beta cell systems, KDAC inhibitors were found to modulate KDAC expression [32]. To investigate whether KDAC inhibition is associated with alterations in basal and cytokine-induced expression of selected KDAC genes in beta cells, INS-1 cells were pre-exposed to ITF2357 for 1 h and then to IL-1β and IFNγ for 24 h. ITF2357 did not affect the basal expression of Hdac1 and Hdac2, whereas a minor but significant inhibition was observed on Hdac6 and Hdac11 expression (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…In non-beta cells, the expression of Hdac1 and Hdac6 has been found to be increased upon non-selective KDAC inhibitor exposure [32]. We were not able to reproduce this finding, possibly due to the use of a different experimental model (neuroblastoma cell line vs INS-1 cell line) and a different non-selective KDAC inhibitor in non-comparable concentrations (trichostatin A 0.5 μmol/l vs ITF2357 62.5 and 125 nmol/l).…”

Section: Discussionmentioning

confidence: 99%

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Lysine deacetylases are produced in pancreatic beta cells and are differentially regulated by proinflammatory cytokines

et al. 2010

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Aims/hypothesis Cytokine-induced beta cell toxicity is abrogated by non-selective inhibitors of lysine deacetylases (KDACs). The KDAC family consists of 11 members, namely histone deacetylases HDAC1 to HDAC11, but it is not known which KDAC members play a role in cytokine-mediated beta cell death. The aim of the present study was to examine the KDAC gene expression profile of the beta cell and to investigate whether KDAC expression is regulated by cytokines. In addition, the protective effect of the non-selective KDAC inhibitor ITF2357 and interdependent regulation of four selected KDACs were investigated. Methods The beta cell line INS-1 and intact rat and human islets were exposed to cytokines with or without ITF2357.Expression of mRNA was assessed by real-time PCR and selected targets validated at the protein level by immunoblotting. Effects on cytokine-induced toxicity were investigated by in vitro assays. Results Hdac1 to Hdac11 were expressed and differentially regulated by cytokines in INS-1 cells and rat islets. HDAC1, -2, -6 and -11 were found to be expressed and regulated by cytokines in human islets. ITF2357 protected against cytokine-induced beta cell apoptosis and counteracted cytokine-induced attenuation of basal insulin secretion. In addition, cytokine-induced regulation of Hdac2 and Hdac6, but not Hdac1 and Hdac11, was reduced by KDAC inhibition. Conclusions/interpretation All classical KDAC genes are expressed by beta cells and differentially regulated by L.G. Grunnet and T. Mandrup-Poulsen contributed equally to this work.Electronic supplementary material The online version of this article

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Lysine deacetylases are produced in pancreatic beta cells and are differentially regulated by proinflammatory cytokines

et al. 2010

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“…HDAC inhibitors can induce growth arrest, differentiation, and/or apoptotic cell death in a wide variety of cultured transformed cells, including neuroblastoma (19), melanoma (20), leukemia (21), as well as breast, prostate, lung, ovary, and colon cancers (22). Induction of apoptosis by HDAC inhibitors has been reported in multiple human cancer cell lines, frequently via intrinsic pathway caspase activation (15,23).…”

Section: Discussionmentioning

confidence: 99%

Chronic Administration of Valproic Acid Inhibits Prostate Cancer Cell Growth In vitro and In vivo

et al. 2006

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Valproic acid (VPA) is an established drug in the long-term therapy of seizure disorders. Recently, VPA has been associated with anticancer activity, an effect thought to be mediated through the inhibition of cellular histone deacetylase 1. We investigated the effect of various doses of VPA (0, 1.2, and 5.0 mmol/L) administered either acutely or chronically on histone acetylation, p21 gene expression, androgen receptor expression, prostate-specific antigen (PSA) expression, and cell survival and proliferation in prostate cancer cell lines. We also studied the effect of chronic VPA on tumor xenograft growth in vivo. Our results show that acute treatment (3 days) VPA can increase net histone H3 acetylation and up-regulate p21, AR, and cytosolic PSA expression. Interestingly, the effects on AR and PSA are reversed with chronic teatment. In addition, acute VPA reduces cell survival but has no effect on the subsequent proliferation of surviving cells following drug withdrawal. However, when VPA is chronically administered (10-14 days) to prostate cancer cells, even lower doses of VPA result in marked decreases in the net proliferation rate, correlating with increased caspase-2 and caspase-3 activation. These effects are evident in both androgen receptor-positive (LNCaP and C4-2) and androgen receptor-negative (DU145 and PC3) prostate cancer cells. Moreover, chronic VPA treatment results in statistically significant reduction of tumor xenograft growth in vivo. We conclude that acute treatment has nominal effects on prostate cancer cell survival and proliferation, but chronic VPA results in profound decreases in proliferation, independently of androgen regulation. (Cancer Res 2006; 66(14): 7237-44)

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“…Likely candidates would be HDAC2 (Guan et al, 2009) andHDAC3 (McQuown et al, 2011), which act as negative constraints of memory function. In contrast, the administration of TSA to neuronal cells was shown to increase the expression of HDAC1 (Ajamian et al, 2004), which provides another possible explanation why the pan-HDAC inhibitor TSA facilitates fear extinction. Future studies that specifically address the role of HDAC2-11 during fear extinction will be necessary to clarify this issue.…”

Section: Hippocampal Hdac1 Regulates Fear Extinctionmentioning

confidence: 96%

HDAC1 Regulates Fear Extinction in Mice

Bahari‐Javan

Maddalena²,

Kerimoğlu³

et al. 2012

J. Neurosci.

169

140

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Histone acetylation has been implicated with the pathogenesis of neuropsychiatric disorders and targeting histone deacetylases (HDACs) using HDAC inhibitors was shown to be neuroprotective and to initiate neuroregenerative processes. However, little is known about the role of individual HDAC proteins during the pathogenesis of brain diseases. HDAC1 was found to be upregulated in patients suffering from neuropsychiatric diseases. Here, we show that virus-mediated overexpression of neuronal HDAC1 in the adult mouse hippocampus specifically affects the extinction of contextual fear memories, while other cognitive abilities were unaffected. In subsequent experiments we show that under physiological conditions, hippocampal HDAC1 is required for extinction learning via a mechanism that involves H3K9 deacetylation and subsequent trimethylation of target genes. In conclusion, our data show that hippocampal HDAC1 has a specific role in memory function.

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Selective regulation of class I and class II histone deacetylases expression by inhibitors of histone deacetylases in cultured mouse neural cells

Cited by 39 publications

References 19 publications

Lysine deacetylases are produced in pancreatic beta cells and are differentially regulated by proinflammatory cytokines

Lysine deacetylases are produced in pancreatic beta cells and are differentially regulated by proinflammatory cytokines

Chronic Administration of Valproic Acid Inhibits Prostate Cancer Cell Growth In vitro and In vivo

HDAC1 Regulates Fear Extinction in Mice

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