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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
	SRR19607677.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

Thyroid hormone regulated genes in the neonatal testis

Project description:An excess in thyroid hormone during rodent neonatal life causes abnormal prolifration and maturation of testicular cells, leading to reduced testis size and impairments in steroidogenesis, Sertoli cell function, spermatogenesis and fertility. The high expression of type 3 deiodinase in the neonatal testis protects this tissue from premature exposure to thyroid hormones, since this gene (Dio3) function is to degrade thyroid hormones. DIO3-deficient mice (Dio3KO) exhibit a marked reduction in Sertoli cell proliferation and testis size, abnormalities in the reproductive axis and impaired fertility (Martinez et al. 2016, Endocrinology157:1276). To identify genes that are untimely regulated by thyroid hormone in the developing testes, we have performed RNAseq in testis total RNA from wild type and DIO3KO mouse neonates.

2019-08-01 | GSE117157 | 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

2022-11-23 | GSE198416 | GEO

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

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

| PRJNA815050 | ENA

Analysis of the retinal gene expression after hypoxic preconditioning identifies candidate genes for neuroprotection

Project description:Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1α in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. Our data suggest that neuroprotection after hypoxic preconditioning of the retina is the result of the differential expression of a multitude of genes which may act in concert to protect visual cells against a toxic insult. Keywords: hypoxic preconditioning, neuroprotection, transcription-profile, retina

2009-01-10 | GSE14366 | GEO

Transcription profiling of mouse retinal gene expression after hypoxic preconditioning identifies candidate genes for neuroprotection

Project description:Neuroprotective therapies for retinal degeneration may be used to rescue retinal cells and preserve vision. Hypoxic preconditioning stabilizes the transcription factor HIF-1Î± in the retina and strongly protects photoreceptors in an animal model of light-induced retinal degeneration. Our data suggest that neuroprotection after hypoxic preconditioning of the retina is the result of the differential expression of a multitude of genes which may act in concert to protect visual cells against a toxic insult. Experiment Overall Design: In total 24 samples were analyzed on Affymetrix mouse 430.2 arrays, the samples represent different durations of regeneration (none = 0 h, 2 h, 4 h and 16 h) from hypoxic or normoxic treatments, that were tested in triplicates.

2009-01-17 | E-GEOD-14366 | biostudies-arrayexpress

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

Project description:Thyroid hormone receptor beta (THRB) is post-translationally modified by small ubiquitin-like modifier (SUMO). To investigate the biological role of THRB sumoylation, we generated a mouse model with a mutation that disrupts sumoylation at lysine 146 (K146Q). The THRB K146Q mutant mice had normal serum thyroxine (T4), markedly elevated serum thyrotropin (TSH) (81-fold above control), and enlargement of both the pituitary and the thyroid gland. The marked elevation in TSH, despite a normal serum T4 concentration, indicated blunted feedback regulation of TSH. TH profuction was 10-fold lower (per mg of thyroid tissue) in mutant mice compared to Wt mice.

2021-02-20 | GSE167105 | GEO

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

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