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Thyroid hormone-mediated histone modificaiton protects primary mouse cortical neurons from the toxic effects of hypoxic injury.

ABSTRACT: Thyroid hormone-mediated histone modificaiton protects primary mouse cortical neurons from the toxic effects of hypoxic injury.

PROVIDER: PRJNA847627 | ENA |

REPOSITORIES: ENA

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	SRR19607674.fastq.gz	Fastqsanger.gz
	SRR19607675.fastq.gz	Fastqsanger.gz
	SRR19607676.fastq.gz	Fastqsanger.gz
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Thyroid hormone-mediated histone modificaiton protects primary mouse cortical neurons from the toxic effects of hypoxic injury.

Project description:Epigenetic and genetic regulation mediates the response to stress at the cellular level and allows cells for adaptation and survival. Thyroid hormone has been shown to have a protective role in neuronal injury, although the mechanisms are not established. We hypothesized that the neuroprotective role of thyroid hormone was associated with epigenetic modifications of histone proteins. We used hypoxic neurons as a model system for hypoxia-induced brain injury. Mouse primary cortical neurons were exposed to 0.2% oxygen for 7 hours with or without treatment with 10 nM Triiodotyroxine (T3). We analyzed the mRNA expression of histone modifying enzymes by RNA-seq and the posttranslationally modified histone 3 proteins by ELISA assay and Western blot. We found that methylation of H3K27, associated with inactive promoters, was highly induced in hypoxic neurons, and this methylation was reduced by T3 treatment. H3K4 methylation is the hallmark of active promoters. Three (Set1db, Kmta2c and Kmt2e) out of six H3K4 methyltransferases were downregulated by hypoxia and restored by T3 treatment. H3K4me3 protein, by ELISA assay, was increased 76% in T3-treated hypoxic neurons, compared to without T3 treatment. H3K56ac, plays a critical role in transcription initiation, was markedly increased in T3-treaed hypoxic neurons, compared to those without T3 treatment, indicating that T3 treatment stimulated gene transcription. Additionally, T3 treatment restored hypoxia-induced downregulation of histone acetyltransferase, Kat6a, Kat6b and Crebbp, which function as transcription factors. These findings indicate that T3 treatment mitigates hypoxia-induced alteration of the histone modifications and protects neurons from hypoxia-induced injury.

2022-07-27 | GSE205801 | GEO

Thyroid Hormone-mediated Histone Modification Protects Cortical Neurons From the Toxic Effects of Hypoxic Injury.

Project description:ContextThyroid hormone has been shown to have a protective role in neuronal injury, although the mechanisms have not been established. The cellular response to stress that promotes adaptation and survival has been shown to involve epigenetic modifications.ObjectiveWe hypothesized that the neuroprotective role of thyroid hormone was associated with epigenetic modifications of histone proteins. We used hypoxic neurons as a model system for hypoxia-induced brain injury.MethodsMouse primary cortical neurons were exposed to 0.2% oxygen for 7 hours, with or without, treatment with triiodothyronine (T3). We analyzed the expression of histone-modifying enzymes by RNA-seq and the post-translationally modified histone 3 proteins by enzyme-linked immunosorbent assay (ELISA) and Western blot.ResultsWe found that methylation of H3K27, associated with inactive promoters, was highly induced in hypoxic neurons, and this histone methylation was reduced by T3 treatment. H3K4 methylation is the hallmark of active promoters. The expression of 3 (Set1db, Kmta2c, and Kmt2e) out of 6 H3K4 methyltransferases was downregulated by hypoxia and expression was restored by T3 treatment. H3K4me3 protein, measured by ELISA, was increased 76% in T3-treated hypoxic neurons compared with the levels without T3 treatment. H3K56ac plays a critical role in transcription initiation and was markedly increased in T3-treated hypoxic neurons compared with those without T3 treatment, indicating stimulation of gene transcription. Additionally, T3 treatment restored hypoxia-induced downregulation of histone acetyltransferase, Kat6a, Kat6b, and Crebbp, which function as transcription factors.ConclusionThese findings indicate that T3 treatment mitigates hypoxia-induced histone modifications and protects neurons from hypoxia-induced injury.

| S-EPMC9562813 | biostudies-literature

Knockout of thyroid hormone receptor alpha a (thraa) enhances cardiac regeneration in zebrafish through metabolic and hypoxic regulation

Project description:Thyroid hormone (TH) serves as a master regulator in our body, governing body metabolism and growth. Circulating TH level has been demonstrated to correlate with cardiac regenerative potential by modulating cell-cycle arrest and polyploidization in cardiomyocytes (CMs), while the molecular mechanism is still unknown. Here, we investigated the molecular mechanisms of TH signalling on heart regeneration through a time-course sequencing experiment. We disrupted the TH signalling in a zebrafish model by thyroid hormone receptor alpha a (thraa) knockout (KO). The thraa-KO zebrafish demonstrated an accelerated heart regenerative process, indicating that TH through thyroid hormone receptors (TRs) impaired heart regeneration. Our study discovered that diminished TH signalling in thraa-KO zebrafish alters the pro-inflammatory response and the regenerative process of cardiac tissue through myocardial metabolic switch. Moreover, TH signalling was shown to modulate the restoration of hypoxic response via hif3a. Altogether, our study highlighted that the role of TH signalling in modulating the progress of heart regeneration in zebrafish.

2025-07-16 | GSE282482 | GEO

The thyroid hormone clearing type 3 deiodinase protects from cardiac congenital abnormalities

Project description:We examined the impact of thyroid hormone excess on the mouse fetal heart utilizing a model of deficiency in DIO3, the enzyme that is responsible for clearing thyroid hormones

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Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

Project description:Thyroid hormone receptor beta is required for thyrotrpin regulation and thyroid hormone production.

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

Project description:Using tadpoles mutant for thyroid hormone receptor alpha (thra), we show that TRa is required for thyroid hormone (T3) induction of cell proliferation in the brain. RNA-sequencing showed that the TRa is required for 95% of the gene regulation responses to T3.

2019-05-13 | GSE130816 | GEO

Thyroid hormone receptor a in skeletal muscle is essential for thyroid thermogenesis

Project description:Thyroid hormones are important for homeostatic control of energy metabolism and body temperature. Although skeletal muscle is considered an important site for thyroid action, the contribution of thyroid hormone receptor signaling, in muscle, to whole-body energy metabolism and body temperature has not been resolved. Here, we show that thyroid hormone-induced increase in energy expenditure requires thyroid hormone receptor alpha 1 (TRa1) in skeletal muscle, but that thyroid hormone induced elevation in body temperature is independent of muscle-TRa1. In slow-twitch soleus muscle, ablation of TRa1 leads to an altered fiber type composition toward a more oxidative phenotype, which, however, does not influence running capacity or motivation to voluntary running. RNA-sequencing of soleus muscle from WT mice and TRaHSACre mice revealed differentiated transcriptional regulation of genes associated with muscle thermogenesis, such as sarcolipin and UCP3, thus providing molecular clues pertaining to the mechanistic underpinnings of TRa1-linked control of whole-body metabolic rate. Together, this work establishes a fundamental role for skeletal muscle in thyroid hormone-stimulated increase in whole-body energy expenditure.

2020-09-21 | GSE146336 | GEO

Target genes of thyroid hormone in cerebellum neurons

Project description:Cerebellar post-natal development is particularly sensitive to thyroid hormone and low levels of thyroid hormone (hypothyroidism) result in permanent defects in cerebellar architecture and function. All cell types of the cerebellum are affected, but the main sign of hypothyroidism in mice is the persistence of the external granular layer, composed of mitotic neuronal precursors at P21. To make the genetic link between thyroid hormone and cerebellar development, we sought to identify new thyroid hormone target genes, in particular in granule cells which represent the vast majority of cerebellar cells.

2012-03-30 | GSE24793 | GEO

Thyroid Hormone Promotes Fetal Neurogenesis [CosMx]

Project description:Thyroid Hormone Promotes Fetal Neurogenesis [CosMx]

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A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

Project description:A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

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