Thyroid hormones play a central role in Central Nervous System (CNS) development, besides being essential for some of the most important physiologic parameters. Deiodination involves the conversion of T4 into T3, a process catalyzed by D1, D2 and D3 enzymes, which can promote the activation or inactivation of the thyroid hormones in response to the specific needs of the tissues. D3 is responsible for preventing the formation of T3 from T4 and its expression is barely dectable after birth. However, tissues subjected to pathophysiology conditions present a pronounced expression of D3 enzyme, resulting in local hypothyroidism. Therefore, our hypothesis considers that the observed increased D3 expression minimizes the negative effects of the low oxygen supply to the tissues, providing a protective mechanism. Thus, we intend to determine the D3, HIP-1± and Neuroglobin expression by immunohistochemistry, and the mRNA of T3 responsible genes and proteins expression in wild-type mice CNS subjected to ischemic-hypoxia, by real-time PCR and Western Blotting. In order to determine if this effect is involved in a protective mechanism for the brain, all the experiments will be repeated in knockdown mice for the D3 enzyme in the brain (HtzD3KO).Keywords: Type 3 iodothyronine deiodinase; Thyroid hormone, Hypoxic-isquemic.
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