Genome-wide maps of chromatin state(ATAC-seq) and gene expression(RNA-seq) of cold exposed Dot1L-ablated mouse brown adipose tissue
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE159645 | GEO | 2020/11/10
REPOSITORIES: GEO
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Project description:Purpose: We investigated the transcriptomic change in brown fat of young and old mice (wild type) through high-throughput RNA-sequencing (RNA-Seq) analysis when the mice were exposed to cold room or room temperatur. Methods: We prepared 10 of young (3 months) mice and 9 of old (24 months) mice, and kept them in cold room (4°c) or room temperature (24°c) for 24 hours. Then, we sacrified mice and extracted RNA from brown fat tissue (BAT) for RNA-seq experiment. Results: BAT of Young mice showed increased carbohydrate metabolism and glycolytic flux during cold exposure Conclusions: The thermogenesis function of BAT is accelerated on cold exposure.
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Project description:Cold stimulation dynamically remodels mitochondria in brown adipose tissue (BAT) to facilitate non-shivering thermogenesis in mammals, but what regulates mitochondrial plasticity is poorly understood. Comparing mitochondrial proteomes in response to cold identify FAM210A as a cold-inducible mitochondrial inner membrane protein. Adipocyte-specific constitutive knockout of Fam210a (Fam210aAKO) disrupts mitochondrial cristae structure and diminishes the thermogenic activity of BAT, rendering the Fam210aAKO mice lethal hyperthermia under acute cold exposure. Induced knockout of Fam210a in adult adipocytes (Fam210aiAKO) does not affect steady-state, non-thermogenic mitochondria under thermoneutrality, but impairs cold-induced mitochondrial remodeling, leading to progressive loss of cristae and reduction of mitochondrial density. Proteomics reveals an association between FAM210A and OPA1, whose cleavage governs cristae dynamics and mitochondrial remodeling. Mechanistically, FAM210A interacts with mitochondrial protease YME1L and modulates its activity toward OMA1 and OPA1 cleavage. These data establish FAM210A as a key regulator of mitochondrial cristae remodeling in BAT and shed light on the mechanism underlying mitochondrial plasticity in response to cold.
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Project description:<p>Glucose uptake is essential for cancer glycolysis and is involved in non-shivering thermogenesis of adipose tissues. Most cancers use glycolysis to harness energy for their infinite growth, invasion and metastasis. Activation of thermogenic metabolism in brown adipose tissue (BAT) by cold and drugs instigates blood glucose uptake in adipocytes. However, the functional effects of the global metabolic changes associated with BAT activation on tumour growth are unclear. Here we show that exposure of tumour-bearing mice to cold conditions markedly inhibits the growth of various types of solid tumours, including clinically untreatable cancers such as pancreatic cancers. Mechanistically, cold-induced BAT activation substantially decreases blood glucose and impedes the glycolysis-based metabolism in cancer cells. The removal of BAT and feeding on a high-glucose diet under cold exposure restore tumour growth, and genetic deletion of Ucp1-the key mediator for BAT-thermogenesis-ablates the cold-triggered anticancer effect. In a pilot human study, mild cold exposure activates a substantial amount of BAT in both healthy humans and a patient with cancer with mitigated glucose uptake in the tumour tissue. These findings provide a previously undescribed concept and paradigm for cancer therapy that uses a simple and effective approach. We anticipate that cold exposure and activation of BAT through any other approach, such as drugs and devices either alone or in combination with other anticancer therapeutics, will provide a general approach for the effective treatment of various cancers.</p>
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Project description:Deficiency of the epigenome modulator histone deacetylase 3 (HDAC3) in brown adipose tissue (BAT) impairs the ability of mice to survive in near-freezing temperatures. Here, we report that short-term exposure to mild cold temperature (STEMCT: 15°C for 24 hours) averted lethal hypothermia of mice lacking HDAC3 in BAT (HDAC3 BAT KO) exposed to 4°C. STEMCT restored the induction of the thermogenic coactivator PGC-1a along with UCP1 at 22°C, which is greatly impaired in HDAC3-deficient BAT, and deletion of either UCP1 or PGC-1a prevented the protective effect of STEMCT. Remarkably, the protection of HDAC3 BAT KO mice from cold intolerance following STEMCT lasted for up to 7 days. Transcriptional activator C/EBPb was induced by short-term cold exposure in mouse and human BAT and, uniquely, remained high for 7 days following STEMCT. Furthermore, analysis of C/EBPb activity revealed increased binding following STEMCT at genes, including the enhancers/promotors of UCP1 and PGC-1a. These results reveal the existence of a cold-adaptive epigenomic memory mediated by C/EBPb that is persistent and HDAC3-independent.
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Project description:Deficiency of the epigenome modulator histone deacetylase 3 (HDAC3) in brown adipose tissue (BAT) impairs the ability of mice to survive in near-freezing temperatures. Here, we report that short-term exposure to mild cold temperature (STEMCT: 15°C for 24 hours) averted lethal hypothermia of mice lacking HDAC3 in BAT (HDAC3 BAT KO) exposed to 4°C. STEMCT restored the induction of the thermogenic coactivator PGC-1a along with UCP1 at 22°C, which is greatly impaired in HDAC3-deficient BAT, and deletion of either UCP1 or PGC-1a prevented the protective effect of STEMCT. Remarkably, the protection of HDAC3 BAT KO mice from cold intolerance following STEMCT lasted for up to 7 days. Transcriptional activator C/EBPb was induced by short-term cold exposure in mouse and human BAT and, uniquely, remained high for 7 days following STEMCT. Furthermore, analysis of C/EBPb activity revealed increased binding following STEMCT at genes, including the enhancers/promotors of UCP1 and PGC-1a. These results reveal the existence of a cold-adaptive epigenomic memory mediated by C/EBPb that is persistent and HDAC3-independent.
2024-07-05 | GSE244383 | GEO
Project description:Deficiency of the epigenome modulator histone deacetylase 3 (HDAC3) in brown adipose tissue (BAT) impairs the ability of mice to survive in near-freezing temperatures. Here, we report that short-term exposure to mild cold temperature (STEMCT: 15°C for 24 hours) averted lethal hypothermia of mice lacking HDAC3 in BAT (HDAC3 BAT KO) exposed to 4°C. STEMCT restored the induction of the thermogenic coactivator PGC-1a along with UCP1 at 22°C, which is greatly impaired in HDAC3-deficient BAT, and deletion of either UCP1 or PGC-1a prevented the protective effect of STEMCT. Remarkably, the protection of HDAC3 BAT KO mice from cold intolerance following STEMCT lasted for up to 7 days. Transcriptional activator C/EBPb was induced by short-term cold exposure in mouse and human BAT and, uniquely, remained high for 7 days following STEMCT. Furthermore, analysis of C/EBPb activity revealed increased binding following STEMCT at genes, including the enhancers/promotors of UCP1 and PGC-1a. These results reveal the existence of a cold-adaptive epigenomic memory mediated by C/EBPb that is persistent and HDAC3-independent.
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