[Thyroid hormones and muscle phenotype: involvement of new signaling pathways].

Journal de la Societe de biologie Pub Date : 2008-01-01 Epub Date: 2008-06-13 DOI:10.1051/jbio:2008011
André-Xavier Bigard, Nathalie Koulmann, Lahoucine Bahi, Hervé Sanchez, Renée Ventura-Clapier
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引用次数: 2

Abstract

Thyroid hormones (TH) are known to control development, body and muscle growth, as well as to determine muscle phenotype in the adult. TH affect muscle properties through nuclear receptors; they act either by a positive or a negative control on target genes that encode proteins accounting for contractile or metabolic phenotypes. Contractile activity and muscle load also affect muscle phenotype; several intracellular signaling pathways are involved in the transduction of signals related to contractile activity, including the calcineurin/NFAT pathway. Calcineurin activity is negatively controlled by MCIP-1 protein (modulatory calcineurin-interacting protein-1). We recently performed an experiment aimed at examining the specific and combined effects of the pharmacological calcineurin inhibition (using cyclosporin-A CsA administration) and thyroid hormone deficiency. The expected effects of CsA administration were only observed if TH were available, while thyroid deficiency totally blunted the muscle responses to calcineurin inhibition. In conditions of thyroid hormone deficiency, there was no response to the pharmacological inhibition of calcineurin, usually known to induce a slow-to-fast IIA transition associated with an enhancement of mitochondrial biogenesis in normothyroid rats. Moreover, thyroid deficiency markedly decreased the expression of MCIP-1 and MCIP-2 mRNA and proteins, two endogenous calcineurin inhibitors; such results clearly suggest that thyroid hormone and calcineurin pathways are interconnected.

[甲状腺激素和肌肉表型:新信号通路的参与]。
众所周知,甲状腺激素(TH)控制发育、身体和肌肉生长,并决定成年人的肌肉表型。TH通过核受体影响肌肉特性;它们通过对目标基因的积极或消极控制来发挥作用,这些基因编码的蛋白质负责收缩或代谢表型。收缩活动和肌肉负荷也影响肌肉表型;一些细胞内信号通路参与与收缩活动相关的信号转导,包括钙调神经磷酸酶/NFAT通路。钙调神经磷酸酶活性受MCIP-1蛋白(调节性钙调神经磷酸酶相互作用蛋白-1)负调控。我们最近进行了一项实验,旨在检查药物钙调磷酸酶抑制(使用环孢素- a CsA)和甲状腺激素缺乏的特异性和联合效应。CsA给药的预期效果仅在有TH的情况下观察到,而甲状腺缺乏完全钝化了肌肉对钙调磷酸酶抑制的反应。在甲状腺激素缺乏的情况下,对钙调神经磷酸酶的药理学抑制没有反应,钙调神经磷酸酶通常在正常甲状腺大鼠中诱导缓慢到快速的IIA转变,并增强线粒体生物发生。此外,甲状腺缺乏显著降低内源性钙调磷酸酶抑制剂MCIP-1和MCIP-2 mRNA和蛋白的表达;这些结果清楚地表明,甲状腺激素和钙调磷酸酶途径是相互关联的。
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