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首页> 外文期刊>Life sciences >L-triiodothyronine differentially and nongenomically regulates synaptosomal protein phosphorylation in adult rat brain cerebral cortex: Role of calcium and calmodulin
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L-triiodothyronine differentially and nongenomically regulates synaptosomal protein phosphorylation in adult rat brain cerebral cortex: Role of calcium and calmodulin

机译：L-triiodothyronine差异和非基因组调节成年大鼠大脑皮质的突触体蛋白磷酸化：钙和钙调蛋白的作用。

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Adult-onset thyroid disorders in humans impair several important central nervous system functions, causing various neuropsychiatric diseases. However, the mechanisms of thyroid hormone (TH) action in the mature mammalian brain remain unclear. Recent nongenomic actions of TH in adult brains are spotlighted. Many nongenomic mechanisms are modulated by phosphorylation-dephosphorylation of substrate proteins. In the present study, L-triiodothyronine (L-T3) demonstrated differential regulation of phosphorylation status of five 21 different synaptosomal proteins (63, 53, 38, 23, and 16 kD) in both a Ca2+/calmodulin (CaM)-dependent and -independent manner. L-T3 increased the level of phosphorylation of all these five proteins. Ca2+/CaM further stimulated phosphorylation of 63- and 53-kD proteins by L-T3, which were inhibited both by EGTA (Ca2+- chelator) or KN62 (Ca2+/CaM kinase-11 [CaMK-II] inhibitor), suggesting the role of CaMIK-II. L-T3 increased the phosphorylation of 23- and 38-kD proteins; the effect was independent of EGTA or KN62. The presence of Ca2+ decreased L-T3-induced phosphorylation of 63-, 53- and 38-kD proteins. Surprisingly, L-T3-induced phosphorylation of 16-kD protein was not augmented further with Ca2+ or Ca2+/CaM; instead, the presence of CaM abolished the L-T3-induced phosphorylation. EGTA or KN62 could not restore the effect of CaM-induced dephosphorylation of this protein. This study identified the role of Ca2+/CaM in the regulation of L-T3-induced protein phosphorylation and supported a unique nongenomic mechanism of second messenger-mediated regulation of protein phosphorylation by TH in mature rat brain. This has profound implications for higher mental functions and strategies for novel therapeutics. (c) 2008 Elsevier Inc. All rights reserved.
机译：人类的成人甲状腺疾病会损害一些重要的中枢神经系统功能，导致各种神经精神疾病。然而，在成熟的哺乳动物脑中甲状腺激素（TH）的作用机制仍不清楚。 TH在成人大脑中的最新非基因组作用受到关注。许多非基因组机制是通过底物蛋白的磷酸化-去磷酸化来调节的。在本研究中，L-三碘甲腺氨酸（L-T3）在依赖Ca2 + /钙调蛋白（CaM）的蛋白和钙调蛋白（CaM）中均显示了5种21种不同突触蛋白（63、53、38、23和16 kD）磷酸化状态的差异调节。 -独立方式。 L-T3增加了所有这五个蛋白质的磷酸化水平。 Ca2 + / CaM通过L-T3进一步刺激了63-和53-kD蛋白的磷酸化，这被EGTA（Ca2 +-螯合剂）或KN62（Ca2 + / CaM激酶-11 [CaMK-II]抑制剂）抑制。 CaMIK-II。 L-T3增加23-kD和38-kD蛋白的磷酸化。该效果独立于EGTA或KN62。 Ca2 +的存在降低了L-T3诱导的63-，53-和38-kD蛋白的磷酸化。令人惊讶的是，Ca2 +或Ca2 + / CaM并没有进一步增强L-T3诱导的16-kD蛋白的磷酸化。相反，CaM的存在消除了L-T3诱导的磷酸化。 EGTA或KN62无法恢复CaM诱导的该蛋白去磷酸化的作用。这项研究确定了Ca2 + / CaM在调节L-T3诱导的蛋白磷酸化中的作用，并支持了第二种信使介导的TH在成熟大鼠脑中介导的蛋白磷酸化的独特非基因组机制。这对于更高的心理功能和新型疗法的策略具有深远的意义。 （c）2008 Elsevier Inc.保留所有权利。

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