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

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

PROVIDER: PRJNA1188996 | ENA |

REPOSITORIES: ENA

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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.

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

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Digital Gene Expression (DGE) of thyroid hormone (T3)-responsive genes in C17.2 cells stably transfected with thyroid hormone receptors alpha and beta

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. Cells were treated with 10-7 M T3 for 6, 12 or 24h or left untreated. We performed DGE by sequencing all polyA RNA according to a SAGE-derived method. Differential gene expression after T3 treatment was computed and the T3 responses induced by the two receptors were compared. We could conclude that, in a similar environment, target genes are only partially shared and that a significant proportion show receptor preference and even selectivity. Examination of thyroid hormone target genes over time in two cell lines (C17.2a, C17.2b), each expressing one of the thyroid hormone receptors (alpha, beta).

2012-12-31 | E-GEOD-38539 | biostudies-arrayexpress

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Genome-wide cistromes of thyroid hormone receptors alpha and beta in C17.2 cells

Project description:Tagged versions of thyroid hormone receptors alpha (TRa) and beta (TRb) were stably transfected in two C17.2 cell lines, C17.2a and C17.2b, respectively. We performed an affinity-based purification of chromatin (ChAP), and high-throughput sequencing was used to assess binding sites of both receptors (ChAP-Seq). Standard ChIP-Seq for RXR was also performed in C17.2a cells. These data allow us to compare binding sites for both receptors and to conclude that they were only partially redundant, with co-existence of receptor-specific sites. Examination of binding sites of the two thyroid hormone receptors (alpha, beta) in two cell lines (C17.2a, C17.2b), each expressing one of the receptors. Examination of RXR binding sites in C17.2a cells.

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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.

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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.

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