Methyl CpG level at distal part of heat‐shock protein promoter <i><scp>HSP</scp>70</i> exhibits epigenetic memory for heat stress by modulating recruitment of <scp>POU</scp>2F1‐associated nucleosome‐remodeling deacetylase (Nu<scp>RD</scp>) complex

Kisliouk, Tatiana; Cramer, Tomer; Meiri, Noam

doi:10.1111/jnc.14014

Cited by 40 publications

(30 citation statements)

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“…Heat challenge was performed as previously described (Kisliouk et al, 2017). Briefly, on day 10 post-hatch, both control and EHC experimental chick groups were thermally challenged by exposure to 36 • C for 24 h. The chicks' baseline body temperature was measured and they were sacrificed by decapitation 0, 2, 6, and 24 h into the heat challenge.…”

Section: Experimental Model and Subject Detailsmentioning

confidence: 99%

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Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

et al. 2020

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Early life encounters with stress can lead to long-lasting beneficial alterations in the response to various stressors, known as cross-tolerance. Embryonic heat conditioning (EHC) of chicks was previously shown to mediate resilience to heat stress later in life. Here we demonstrate that EHC can induce cross-tolerance with the immune system, attenuating hypothalamic inflammation. Inflammation in EHC chicks was manifested, following lipopolysaccharide (LPS) challenge on day 10 post-hatch, by reduced febrile response and reduced expression of LITAF and NFκB compared to controls, as well as nuclear localization and activation of NFκB in the hypothalamus. Since the crosstolerance effect was long-lasting, we assumed that epigenetic mechanisms are involved. We focused on the role of ten-eleven translocation (TET) family enzymes, which are the mediators of active CpG demethylation. Here, TET transcription during early life stress was found to be necessary for stress resilience later in life. The expression of the TET family enzymes in the midbrain during conditioning increased in parallel to an elevation in concentration of their cofactor α-ketoglutarate. In-ovo inhibition of TET activity during EHC, by the α-ketoglutarate inhibitor bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl) ethyl sulfide (BPTES), resulted in reduced total and locus specific CpG demethylation in 10-day-old chicks and reversed both thermal and inflammatory resilience. In addition, EHC attenuated the elevation in expression of the stress markers HSP70, CRHR1, and CRHR2, during heat challenge on day 10 post-hatch. This reduction in expression was reversed by BPTES. Similarly, the EHC-dependent reduction of inflammatory gene expression during LPS challenge was eliminated in BPTES-treated chicks. Thus, TET family enzymes and CpG demethylation are essential for the embryonic induction of stress cross-tolerance in the hypothalamus.

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Section: Experimental Model and Subject Detailsmentioning

confidence: 99%

“…There was no sample size calculation. Nevertheless, the sample size was determined on the basis of previous studies (Kisliouk et al, 2017;Cramer et al, 2018). Sample number (n) included the number of individual chicks in each treatment group (indicated in Figure Legends).…”

Section: Quantification and Statistical Analysismentioning

confidence: 99%

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

et al. 2020

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“…The distal portion of the promoter region of HSP70 is aberrantly methylated during thermal stress, restricting the binding of POU class 2 homeobox-1 (POU2F1) to the HSP70 promoter ( 51 ). In T cells, the role of POU2F1 has been shown to contribute to the timing of cytokine expression in CD4 T cells and has also been shown to promote the development of effector T cell lineages ( 52 ).…”

Section: Epigenetic Regulation Of Icd Hallmarksmentioning

confidence: 99%

Dying to Be Noticed: Epigenetic Regulation of Immunogenic Cell Death for Cancer Immunotherapy

et al. 2018

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Immunogenic cell death (ICD) activates both innate and adaptive arms of the immune system during apoptotic cancer cell death. With respect to cancer immunotherapy, the process of ICD elicits enhanced adjuvanticity and antigenicity from dying cancer cells and consequently, promotes the development of clinically desired antitumor immunity. Cancer ICD requires the presentation of various “hallmarks” of immunomodulation, which include the cell-surface translocation of calreticulin, production of type I interferons, and release of high-mobility group box-1 and ATP, which through their compatible actions induce an immune response against cancer cells. Interestingly, recent reports investigating the use of epigenetic modifying drugs as anticancer therapeutics have identified several connections to ICD hallmarks. Epigenetic modifiers have a direct effect on cell viability and appear to fundamentally change the immunogenic properties of cancer cells, by actively subverting tumor microenvironment-associated immunoevasion and aiding in the development of an antitumor immune response. In this review, we critically discuss the current evidence that identifies direct links between epigenetic modifications and ICD hallmarks, and put forward an otherwise poorly understood role for epigenetic drugs as ICD inducers. We further discuss potential therapeutic innovations that aim to induce ICD during epigenetic drug therapy, generating highly efficacious cancer immunotherapies.

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“…Heat stress can epigenetically disrupt HSP70 gene expression triggering immediate and long‐term effects that modulate a future response to stress. Kisliouk, Cramer, and Meiri () observed a higher methylation level at HSP70 promoter in the hypothalamus of harsh‐temperature‐conditioned chicks (40°C for 3 days) compared with control animals conditioned at 36°C. The long‐term effect of such high temperature exposure was observed later in life under heat stress conditions.…”

Section: Heat‐induced Epigenetic Changes In Early Embryonic Developmentmentioning

confidence: 98%

Cellular and epigenetic changes induced by heat stress in bovine preimplantation embryos

Barros

Paula-Lopes

2018

Molecular Reproduction Devel

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Exposure of the preimplantation embryo to heat stress triggers a series of cellular, molecular, and adaptive changes preventing a normal embryonic development. Heat stress disrupts the embryo cytoskeleton, intracellular calcium levels, mitochondrial function, and induces apoptosis. Moreover, heat stress can act indirectly through induction of reactive oxygen species (ROS), leading to a variety of cellular damage. Embryonic resistance to heat shock is determined by factors such as genotype, developmental stage, apoptosis, redox status, and regulatory molecules. The early embryo is very susceptible to heat stress; it acquires resistance to elevated temperature as development advances. One of the mechanisms involved in the developmental acquisition of thermotolerance is heat-induced apoptosis, which acts as a quality control mechanism to remove damaged blastomeres allowing the embryo to survive after stress. Although embryos at >8-cell stage can activate the apoptotic cascade as an adaptive response to stress, embryos at the two-cell stage are resistant to proapoptotic signals. This lack of apoptotic response has been associated to mitochondrial resistance to depolarization and epigenetic regulations, such as DNA methylation and histone deacetylation. Even though the cellular mechanisms triggered by heat stress have been studied, very little attention has been paid to the vulnerability of the epigenome to drastic temperature changes during the preimplantation period. Therefore, this review aims to characterize the effects of elevated temperature on the bovine embryo, especially addresissing developmental, cellular, and epigenetic alterations triggered in response to temperature.

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Methyl CpG level at distal part of heat‐shock protein promoter HSP70 exhibits epigenetic memory for heat stress by modulating recruitment of POU2F1‐associated nucleosome‐remodeling deacetylase (NuRD) complex

Cited by 40 publications

References 36 publications

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

Embryonic Heat Conditioning Induces TET-Dependent Cross-Tolerance to Hypothalamic Inflammation Later in Life

Dying to Be Noticed: Epigenetic Regulation of Immunogenic Cell Death for Cancer Immunotherapy

Cellular and epigenetic changes induced by heat stress in bovine preimplantation embryos

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