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A Deiodinase Polymorphism Causes ER-Stress And Hypothyroidism In The Brain

ABSTRACT: A Deiodinase Polymorphism Causes ER-Stress And Hypothyroidism In The Brain

PROVIDER: PRJNA488825 | ENA |

REPOSITORIES: ENA

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A Deiodinase Polymorphism Causes ER-Stress And Hypothyroidism In The Brain

Project description:Expression data from different brain regions of mice Discrete brain areas were studied using an unbiased whole-transcript microarray approach (Ala92-Dio2 homozygotes vs Thr92-Dio2 homozygotes)

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Type 2 deiodinase polymorphism causes ER stress and hypothyroidism in the brain.

Project description: Not available

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

Project description:An imbalance in thyroid hormones (THs) is associated with reversible dementia and Alzheimer’s disease (AD) pathogenesis. Whether hypothyroidism occurs in AD brains and how it affects AD pathology remain largely unknown. Here, we find that reduced conversion of thyroxine (T4) to tri-iodothyronine (T3) in the brain by decreased iodothyronine deiodinase 2 (DIO2) leads to hippocampal hypothyroidism in early AD model mice prior to TH changes in the blood. A TH deficiency causes immune tolerance with decreased phagocytic activity in microglia, thereby aggravating AD pathology. We demonstrate that microglial ecto-5’-nucleotidase (CD73) is reduced in the hypothyroid state and that its inhibition contributes to immune tolerance in microglia. Thus, our data define a molecular mechanism through which decreased conversion of T4 to T3 in the early AD brain, and consequent brain hypothyroidism causes microglial dysfunction and exacerbates AD pathology.

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

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Overnutrition directly impairs thyroid hormone biosynthesis and utilization, causing hypothyroidism, despite remarkable thyroidal adaptations

Project description:Thyroid hormones (THs: T3 and T4) are key regulators of metabolic rate and nutrient metabolism. They are controlled centrally and peripherally in a coordinated manner to elegantly match T3-mediated energy expenditure (EE) to energy availability. Hypothyroidism reduces EE and has long been blamed for obesity; however, emerging evidence suggests that, instead, obesity may drive thyroid dysfunction. Thus, we used a mouse model of diet-induced obesity to determine its direct effects on thyroid histopathology and function, deiodinase activity, and T3 action. Strikingly, overnutrition induced hypothyroidism within 3 weeks. Levels of thyroidal THs and the TH precursor protein thyroglobulin decreased, and ER stress was induced, indicating that thyroid function was directly impaired. We also observed pronounced morphological and vascular expansion in the thyroid. Overnutrition additionally suppressed T4 activation, rendering the mice resistant to T4 and reducing EE. Our findings collectively show that overnutrition deals a double strike to TH biosynthesis and action, despite large efforts to adapt—but, fortunately, thyroid dysfunction in mice can be reversed by weight loss. In humans, BMI correlated with thyroidal vascularization, importantly signaling initial translatability. These studies lay the groundwork for novel obesity therapies that tackle hypothyroidism—which are much-needed, as no current obesity treatment works for everyone.

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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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Project description:Congenital hypothyroidism is a genetic condition in which the thyroid gland fails to produce sufficient thyroid hormone (TH), resulting in metabolic dysfunction and growth retardation. Xb130-/- mice exhibit perturbations of thyrocyte cytoskeleton and polarity, develop postnatal transient growth retardation due to congenital hypothyroidism and leading to multinodular goiter in elderly. To determine the underlying mechanisms, we performed transcriptomic analyses on thyroid glands of mice at three age points – week 2 (W2, before visible growth retardation), W4 (at the nadir of growth), and W12 (immediately before full growth recovery. We compared gene expression between Xb130+/+ and Xb130-/- mice.

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Pathophysiological relevance of deiodinase polymorphism.

Project description: Not available

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