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ECB-ART-44219
Metab Brain Dis 2015 Dec 01;306:1401-8. doi: 10.1007/s11011-015-9718-5.
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Thyroid hormone modulates neuroglobin and cytoglobin in rat brain.

Oliveira KC , da Conceição RR , Piedade GC , de Souza JS , Sato MA , de Barros Maciel RM , Giannocco G .


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Thyroid hormones (THs) are essential and crucial for brain development, playing a role in growth and differentiation. Two globins named neuroglobin (Ngb) and cytoglobin (Cygb) are located in the brain, and each one has different distribution and function: They seem to have similar action by providing O(2) for respiratory chain, and detoxification of reactive oxygen species (ROS) and nitric oxide (NO) protecting tissues against irreversible lesions. We aimed to investigate the influence of thyroid state in Ngb and Cygb metabolism in different brain regions and evaluate their responses in cerebellum, hippocampus and cerebral cortex (hereafter called as cortex) after supraphysiological doses at different time points of TH administration. Experiments were carried out in rats, divided in eight experimental groups Control (C), thyroidectomy (Tx), and thyroidectomy treated with jugular intravenous injection (i.v). T3 (100 μl/100 g) injection and sacrificed after 30, 60, 120 min and 6, 12 and 24 h. In cortex, we found increase in Ngb gene and protein expression in different time points compared to C group, however Cygb gene and protein expression were decreased. In hippocampus, Ngb and Cygb protein expression increased 24 h after i.v. T3 injection in comparison to Tx. In cerebellum, we found increased Ngb gene expression after 120 min, 6, 12 and 24 h after T3 administration compared to Tx, and in contrast, protein expression was found to be significantly increased only 12 and 24 h compared to Tx. Ngb and Cygb expression in brain is influenced by thyroid hormone state both by its lack or excess.

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Genes referenced: LOC763287 ros1

References [+] :
Antao, Neuroglobin overexpression in cultured human neuronal cells protects against hydrogen peroxide insult via activating phosphoinositide-3 kinase and opening the mitochondrial K(ATP) channel. 2010, Pubmed