Temperature homeostasis in mice lacking the p43 mitochondrial T3 receptor

Bertrand‐Gaday, Christelle; Pessemesse, Laurence; Cabello, Gérard; Wrutniak‐Cabello, Chantal; Casas, François

doi:10.1002/1873-3468.12129

Cited by 8 publications

(3 citation statements)

References 33 publications

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“…The overproduction of TH increases energy demand and mitochondrial activity, and as a consequence of the latter, there is an increase in the production of ROS [27]. Several authors have described the presence of T3 receptors in mitochondria [9, 28], whereby the TH could also exert direct actions on mitochondrial activity that contribute to the increase in ROS.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balb/c Mice

Costilla

Delbono

Klecha

et al. 2019

Oxidative Medicine and Cellular Longevity

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Hyperthyroidism is an endocrine disorder characterized by excessive secretion of thyroid hormones T3 and T4. Thyroid hormones exert pleiotropic actions on numerous tissues and induce an overall increase in metabolism, with an increase in energy demand and oxygen consumption. Therefore, the purpose of this study was to investigate the effects of hyperthyroidism on the production of reactive oxygen species (ROS) in lymph node and spleen cells of euthyroid and hyperthyroid mice, analyzing antioxidant mechanisms involved in the restitution of the cellular redox state. For this, thirty female Balb/c (H-2d) mice were randomly divided into two groups: euthyroid (by treatment with placebo) and hyperthyroid (by treatment with 12 mg/l of T4 in drinking water for 30 days). We found a significant increase in ROS and an increase in the genomic and protein expression of the antioxidant enzymes catalase (CAT) and glutathione peroxidase-1 (GPx-1) in lymph node and spleen cells of hyperthyroid mice. In vitro treatment with H2O2 (250 μM) of the lymphoid cells of euthyroid mice increased the expression levels of CAT and GPx-1. The hyperthyroidism increased the phosphorylation levels of Nrf2 (nuclear factor erythroid 2-related factor) and the kinase activity of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK). Additionally, we found an increase in the expression of the classic isoenzymes of PKCα, β and γ. In conclusion, these results indicated that the increase in ROS found in the hyperthyroid state induces the antioxidant enzyme transcription through the activation of the Nrf-2 factor in lymphoid tissues. This shows the influence of hyperthyroidism on the regulation of the cellular antioxidant system.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balb/c Mice

Costilla

Delbono

Klecha

et al. 2019

Oxidative Medicine and Cellular Longevity

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“…To our knowledge, variation in TH receptor expression (either nuclear or mitochondrial) has not been studied in response to temperature variation in birds. In mice and rats, mitochondrial receptor p43overexpression was recently found to be associated with higher Tb (Bertrand-Gaday et al, 2016). In vivo (knockout) and in vitro studies in mice revealed that p43 is associated with mitochondrial biogenesis, activity, mito-nuclear crosstalk and even muscle metabolic and contractive phenotype (reviewed in Wrutniak-Cabello et al, 2017;Wrutniak-Cabello et al, 2018), but similar data is lacking from birds.…”

Section: Endocrine and Molecular Mechanisms Of Thermoregulation In Birdsmentioning

confidence: 99%

Endocrinology of thermoregulation in birds in a changing climate

Ruuskanen¹,

Hsu²,

Nord³

2019

Preprint

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The ability to maintain a (relatively) stable body temperature in a wide range of thermal environments is a unique feature of endotherms such as birds. Endothermy is acquired and regulated via various endocrine and molecular pathways, and ultimately allows wide aerial, aquatic, and terrestrial distribution in variable environments. However, due to our changing climate, birds are faced with potential new challenges for thermoregulation, such as more frequent extreme weather events, lower predictability of climate, and increasing mean temperature. We provide a compact overview on thermoregulation in birds and its endocrine and molecular mechanisms, pinpointing gaps in current knowledge and recent developments, focusing especially on non-model species to understand the generality of, and variation in, mechanisms. We highlight plasticity in thermoregulation and underlying endocrine regulation, because thorough understanding of plasticity is key to predicting responses to changing environmental conditions. To this end, we discuss how changing climate is likely to affect avian thermoregulation and associated endocrine traits, and how the interplay between these physiological processes may play a role in facilitating or constraining adaptation to a changing climate. We conclude that while the general patterns of endocrine regulation of thermogenesis are quite well understood, at least in poultry, the molecular and endocrine mechanisms that regulate e.g. mitochondria function and plasticity of thermoregulation over different time scales (from transgenerational to daily variation) need to be unveiled. Plasticity may ameliorate climate change effects on thermoregulation to some extent, but the increased frequency of extreme weather events, and associated in resource availability, may be beyond the scope and/or speed for plastic responses. This could lead to selection for more tolerant phenotypes, if the underlying physiological traits harbour genetic and individual variation for selection to act on – a key question for future research.

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“…The SC2 and SC7 (n = 87 + 141) displayed highest activity at D0 and then decreased thereafter, suggesting TFs within these clusters are likely involved in maintaining the thermogenic phenotype of BAT. The TFs in SC2 and SC7 overlapped with many known key thermogenic TFs, such as the EBF1 (Angueira et al, 2020), EBF2 (Stine et al, 2016), NFIA (Hiraike et al, 2017), RORA (Auclair et al, 2021), ESSRG (Müller et al, 2020) and THRA (Bertrand-Gaday et al, 2016), explaining their activity at the beginning of thermogenic adaptation in the extrauterine low-temperature environment. As an example, the aggregated decreased footprint signals of EBF2 on the genome were shown in Supplementary Figure S3B.…”

Section: Genome-wide Footprinting Analysis Revealed Sequential Regula...mentioning

confidence: 97%

Dynamics of transcriptome and chromatin accessibility revealed sequential regulation of potential transcription factors during the brown adipose tissue whitening in rabbits

Chen

Xue

et al. 2022

Front. Cell Dev. Biol.

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Brown adipose tissue (BAT) represents a valuable target for treating obesity in humans. BAT losses of thermogenic capacity and gains a “white adipose tissue-like (WAT-like)” phenotype (BAT whitening) under thermoneutral environments, which could lead to potential low therapy responsiveness in BAT-based obesity treatments. However, the epigenetic mechanisms of BAT whitening remain largely unknown. In this study, BATs were collected from rabbits at day0 (D0), D15, D85, and 2 years (Y2). RNA-sequencing (RNA-seq) and the assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) were performed to investigate transcriptome and chromatin accessibility of BATs at the four whitening stages, respectively. Our data showed that many genes and chromatin accessible regions (refer to as “peaks”) were identified as significantly changed during BAT whitening in rabbits. The BAT-selective genes downregulated while WAT-selective genes upregulated from D0 to Y2, and the de novo lipogenesis-related genes reached the highest expression levels at D85. Both the highly expressed genes and accessible regions in Y2 were significantly enriched in immune response-related signal pathways. Analysis of different relationships between peaks and their nearby genes found an increased proportion of the synchronous changes between chromatin accessibility and gene expression during BAT whitening. The synergistic changes between the chromatin accessibility of promoter and the gene expression were found in the key adipose genes. The upregulated genes which contained increased peaks were significantly enriched in the PI3K-Akt signaling pathway, steroid biosynthesis, TGF-beta signaling pathway, osteoclast differentiation, and dilated cardiomyopathy. Moreover, the footprinting analysis suggested that sequential regulation of potential transcription factors (TFs) mediated the loss of thermogenic phenotype and the gain of a WAT-like phenotype of BAT. In conclusion, our study provided the transcriptional and epigenetic frameworks for understanding BAT whitening in rabbits for the first time and might facilitate potential insights into BAT-based obesity treatments.

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Temperature homeostasis in mice lacking the p43 mitochondrial T3 receptor

Cited by 8 publications

References 33 publications

Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balb/c Mice

Oxidative Stress Produced by Hyperthyroidism Status Induces the Antioxidant Enzyme Transcription through the Activation of the Nrf-2 Factor in Lymphoid Tissues of Balb/c Mice

Endocrinology of thermoregulation in birds in a changing climate

Dynamics of transcriptome and chromatin accessibility revealed sequential regulation of potential transcription factors during the brown adipose tissue whitening in rabbits

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