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• W3094551640 abstract "The epigenetic memory of a cell or an organ is recognized when instructions like ‘transcribe’ or ‘do not transcribe’ a gene, associated with chromatin remodelling, maintaining the chromatin-DNA package in a silent or active state, are given. In other words, transcription is altered without any changes to the inherited DNA sequence. These modifications to gene expression influence cell properties and behaviour, determining resilience or vulnerability to recurring events (Cramer et al. 2019). Environmental stress may play a vital role in epigenetic memory. Unfortunately, our knowledge of the impact of environmental heat stress on epigenetic memory is sparse. The publication by Pandolf et al. (1977), reporting that repeated acclimatization following 18 days of acclimatization-decay was profoundly faster than the period required to achieve initial acclimatization, suggesting that acclimatization (and acclimation) has a memory, drew our attention to the possibility that heat stress has epigenetic impacts. Using our established animal model of acclimation-memory we employed the heat shock proteins (HSPs) system as a prototype to determine whether heat-acclimation-memory involves epigenetics. More specifically, we studied histone modifications at the heat shock element (HSE) binding site of the promoters of hsp70 and hsp90 in rat hearts. Our findings that HSPs, Hsf1 and chromatin remodellers are in the gene clusters with altered expression throughout heat acclimation (AC), de-acclimation (DeAC) and re-acclimation (ReAC), in tandem with the physiological loss of the heat acclimated phenotype upon DeAC and its reacquisition following ReAC, provided the rational for our hypothesis that AC memory is linked to chromatin remodelling and epigenetic machinery. AC mediated cardio-protection via cross-tolerance mechanisms, an inseparable feature of heat acclimation, based on shared alerted genes, served as a marker of acclimation (Tetievsky & Horowitz, 2010). We demonstrated that constitutively acetylated histone H4 and the preserved euchromatin state throughout AC-DeAC-ReAC lead to rapid acclimatory memory (2 days upon ReAC (vs. 30 days to achieve initial AC phenotype) due to prompt HSF-1-HSE binding and subsequent activation of the cytoprotective heat shock response (HSR). The DeAC phase demonstrated a continuum of changes in a variety of genes linked to the ambient temperature (Tetievsky & Horowitz, 2010; Tetievsky et al. 2014). Schermann et al. (2018) predicted that heat injured subjects are more susceptible to recurrent heat injury. This prediction highlighted the link between epigenetics and heat stress, suggesting that the balance between resilience and vulnerability was disrupted. Before the report in this issue of The Journal of Physiology by Murray et al. (2021), the only evidence on the epigenetic-heat stress relationship in adults was our work on heat acclimation memory (Tetievsky & Horowitz, 2010; Tetievsky et al. 2014) and the Schnermann et al. study. The investigation by Murray et al. (2021) is the first study using an animal EHS (exertional heat stroke) model, investigating whether epigenetic mechanisms are involved with consistent changes produced by exertional heat stroke. Numerous studies on the role of epigenetics in innate or adaptive memory focus on the immune system. EHS is characterized by immunosuppression, increased susceptibility to viral infection and altered HSR. Accordingly, Murray et al. (2021) investigated whether EHS produces a lasting epigenetic memory in monocytes and whether there are phenotypic alterations consistent with these changes. Initially monocytes, isolated from bone marrow of female mice were analysed for methylation 4 and 30 days after EHS. Many changes were found in the DNA methylome at both time points, including alterations in the promoter regions of genes involved with immune responsiveness. The authors then challenged whole blood at 30 days with lipopolysaccharide (LPS) to measure cytokine secretion. The increase in proinflammatory cytokine IL-6 and inflammatory cytokine TNFα were attenuated in the EHS vs. controls. There were also differential changes in HSP genes: HSP70 decreased and HSP90 was upregulated in response to an in-vitro heat challenge. Collectively, the data presented by Murray et al. (2021) support the hypothesis that EHS induced long-term molecular changes that may be associated with an altered epigenetic profile. In addition to the methylome changes in bone marrow cells per se, these cells interact with other systems, including brain areas that affect behavioural or physiological responses, e.g. the hypophysis-adrenal axis (e.g. Cramer et al. 2019), thereby increasing corticosteroid levels, and also the immune system leading to the attenuation of the anti-inflammatory TNFα. Although Murray et al. (2021) reported elevated corticosteroids for 3–4 days post EHS “possibly sufficient to reprogram the immune cells for extended period”, Cramer et al. (2019), using a model of chicks before establishment of their thermoregulatory system, showed unequivocally that 24 h of exposure to high levels of corticosteroids is sufficient to induce an epigenetic disruption of resilience to severe heat stress and decrease HSP 70kD, the consensus stress protein. The importance of Murray et al.’s investigation stems from the solid evidence that EHS induces long-term epigenetic memory, suppressing the immune system for almost a month, supporting the prediction that heat intolerant subjects are more susceptible to recurrent EHS (Schermann et al. 2018). The rate of decay, or whether there is any decay of the effects of the stressful event, and which systems are affected remain unknown. Taken together, it seems that heat stress affects the epigenetic machinery in a dose dependent manner, where exposure to moderate stress promotes the development of the adapted, resilient phenotype (Tetievsky & Horowitz, 2010; Tetievsky et al. 2014; Cramer et al. 2019), whereas severe stress causes long-lasting damage (Schermann et al. 2018; Murray et al. 2021). None. Sole author. None." @default.
• W3094551640 created "2020-10-29" @default.
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• W3094551640 date "2020-11-03" @default.
• W3094551640 modified "2023-09-25" @default.
• W3094551640 title "Do exertional heat stroke and environmental heat involve epigenetic memory?" @default.
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• W3094551640 doi "https://doi.org/10.1113/jp280928" @default.
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