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Brain gene expression in systemic hypothyroidism and in mouse models of MCT8 deficiency: The Mct8-Oatp1c1-Dio2 triad.

ABSTRACT: Brain gene expression in systemic hypothyroidism and in mouse models of MCT8 deficiency: The Mct8-Oatp1c1-Dio2 triad.

PROVIDER: PRJNA648939 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12331600.fastq.gz	Fastqsanger.gz
	SRR12331601.fastq.gz	Fastqsanger.gz
	SRR12331602.fastq.gz	Fastqsanger.gz
	SRR12331603.fastq.gz	Fastqsanger.gz
	SRR12331604.fastq.gz	Fastqsanger.gz

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Brain gene expression in systemic hypothyroidism and in mouse models of MCT8 deficiency: The Mct8-Oatp1c1-Dio2 triad.

Project description:The monocarboxylate transporter 8 (Mct8) protein is a primary T4 and T3 (TH) transporter. Mutations of the MCT8-encoding, SLC16A2 gene alters thyroid function and thyroid hormone metabolism, and severely impairs neurodevelopment (Allan-Herndon-Dudley syndrome, AHDS). Mct8-deficient mice manifest thyroid alterations but lack neurological signs. It is thought that Mct8 deficiency in mice is compensated by T4 transport through the Slco1c1-encoded organic anion transporter polypeptide 1c1 (Oatp1c1). This allows local brain generation of sufficient T3 by the Dio2-encoded type 2 deiodinase (D2). The Slc16a2/Slco1c1 (MO) and Slc16a2/Dio2 (MD) double knock out mice lacking T4 and T3 transport, or T3 transport and T4 deiodination, would be more approriate models of AHDS. The goal of this work was to compare the cerebral hypothyroidism of systemic hypothyroidism (SH) caused by thyroid gland blockade with that present in the double KOs.

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Brain hypothyroidism leads to immune tolerance in microglia in Alzheimer's disease [scRNA-seq]

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Project description:Children with congenital hypothyroidism (1 in every ~2,500 live births) may develop a dramatic neurological, muscle-skeleton, and metabolic syndrome due to insufficient thyroid hormone (TH) signaling during development 1-3. While the mechanisms involved remain largely unknown, it is well established that the condition is irreversible if treatment is not initiated during the immediate post-natal period. Here we used high-throughput genomic and epigenomic techniques (Hi-C) to generate high-resolution, genome-wide 3D maps of chromatin interaction in mice with developmental liver-specific hypothyroidism (caused by Dio2 inactivation). The neonatal disruption of hepatic TH signaling only minimally affected genomic compartmentalization but caused substantial rearrangements (e.g. shifting or splitting) in thousands of topologically associating domains (TADs). The rearranged TADs contained DNA sites of hypermethylation, areas of reduced chromatin accessibility, and hundreds of repressed genes. In many instances, the enhancer-promoter (E-P) interaction in key repressed genes had been weakened, explaining the permanent change in how the liver handles excess fat or alcohol in the adult mouse 4-6.

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Aberrant Calreticulin expression in articular cartilage of Dio2 deficient mice

Project description:Microarray-data (Illumina MouseWG-6 v2) of knee cartilage of wild-type and Dio2 -/- -mice were re-analyzed to identify differential expressed genes independent of mechanical loading conditions by forced treadmill-running. Differential expression analyses of articular cartilage of Dio2-/- (N = 9) and wild-type-mice (N = 11) while applying a cutoff threshold (P < 0.05 (FDR) and FC > |1,5|) resulted in 1 probe located in Calreticulin (Calr) that was found significantly downregulated in Dio2-/- mice. The beneficial homeostatic state of articular cartilage in Dio2-/- mice is accompanied with significant lower expression of Calr. Functional analyses further showed that upregulation of Calr expression could act as an initiator of cartilage destruction.

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2021-10-06 | GSE181057 | GEO

Phosphorylation of AHR by PLK1 promotes metastasis of LUAD via DIO2-TH signaling

Project description:Metastasis of Lung adenocarcinoma (LUAD) is a major cause of death in patients. Aryl hydrocarbon receptor (AHR) is an important transcription factor involved in the initiation and progression of lung cancer. Polo-like kinase 1 (PLK1), a serine/threonine kinase, is an oncogene that promotes the malignancy of multiple cancer types. Nonetheless, the interaction between these two factors and significance in lung cancer remains to be determined. Here, we demonstrate that PLK1 phosphorylates AHR at S489 in LUAD, which leads to epithelial-mesenchymal transition (EMT) and metastatic events. RNA-seq analyses show that type 2 deiodinase (DIO2) is responsible for EMT and enhanced metastatic potential. DIO2 converts tetraiodothyronine (T4) to triiodothyronine (T3), which then activates thyroid hormone signaling. In vitro and in vivo experiments demonstrate that treatment with T3 or T4 promotes the metastasis of LUAD, whereas depletion of DIO2 or deiodinase inhibitor disrupts this property. Taken together, our results identify the phosphorylation of AHR by PLK1 as a mechanism leading to the progression of LUAD and provide possible therapeutic interventions for this event.

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