Moeller Lars C, Dumitrescu Alexandra M, Walker Robert L, Meltzer Paul S, Refetoff Samuel
Department of Medicine, The University of Chicago, Illinois 60637, USA.
J Clin Endocrinol Metab. 2005 Feb;90(2):936-43. doi: 10.1210/jc.2004-1768. Epub 2004 Oct 26.
Human skin fibroblasts are readily accessible cells for propagation in culture without transformation that can serve for direct pathophysiology studies in subjects with inherited diseases. We thus examined by quantitative fluorescent cDNA microarray analysis the effect of thyroid hormone (TH) on the expression of more than 15,000 genes in fibroblasts of two normal individuals. Fibroblasts from two subjects with resistance to thyroid hormone (RTH) due to mutations in the TH receptor-beta gene were used to confirm the specificity of the hormonal effect by the ability to discriminate between normal cells and cells with a defect in TH action. Microarray analysis identified 148 genes induced by 1.4-fold or more and five genes repressed to 0.7 or less 24 h after treatment with 2 x 10(-9) M T(3). Taking into account duplicate genes, these represented 91 up-regulated and five down-regulated genes, respectively. Confirmation by real-time PCR was obtained in eight of 10 induced and two of three repressed genes that were tested. Further evidence for T(3)-specific induction was provided by a graded dose response absent in fibroblasts from the patients with RTH. The following genes not previously known to be induced by TH were identified and validated: aldo-keto reductase family 1 C1-3, collagen type VI alpha 3, member RAS oncogene family brain antigen RAB3B, platelet phosphofructokinase, hypoxia-inducible factor-1 alpha, and enolase 1 alpha. These genes as well as three known to be TH regulated in other species and found in this study also in human cells (glucose transporter 1, solute carrier family 16 member 3, and basic transcription element-binding protein 1) have a variety of regulatory functions in development and metabolism. TH seems to induce these genes by initiating either genomic or nongenomic mechanisms. Surprisingly, TH-mediated down-regulation of fibroblast growth factor 7 and alcohol dehydrogenase 1B persisted in fibroblasts from patients with RTH. This first systematic study of TH-mediated gene expression in normal human cells identifies several new TH-responsive genes and demonstrates that skin fibroblasts are suitable for the study of TH action in health and disease.
人皮肤成纤维细胞是易于获取的细胞,可在未转化的情况下在培养中增殖,可用于对遗传性疾病患者进行直接病理生理学研究。因此,我们通过定量荧光cDNA微阵列分析,研究了甲状腺激素(TH)对两名正常个体成纤维细胞中15000多个基因表达的影响。使用来自两名因甲状腺激素受体β基因突变而对甲状腺激素抵抗(RTH)的受试者的成纤维细胞,通过区分正常细胞和甲状腺激素作用有缺陷的细胞的能力,来确认激素作用的特异性。微阵列分析确定,在用2×10⁻⁹ M T₃处理24小时后,有148个基因被诱导1.4倍或更多,5个基因被抑制至0.7或更低。考虑到重复基因,这些分别代表91个上调基因和5个下调基因。在测试的10个诱导基因中的8个和3个抑制基因中的2个中,通过实时PCR得到了证实。RTH患者成纤维细胞中不存在分级剂量反应,这为T₃特异性诱导提供了进一步证据。鉴定并验证了以下先前未知由TH诱导的基因:醛酮还原酶家族1 C1 - 3、VI型胶原α3、RAS癌基因家族脑抗原RAB3B、血小板磷酸果糖激酶、缺氧诱导因子-1α和烯醇化酶1α。这些基因以及在其他物种中已知受TH调节且在本研究中也在人类细胞中发现的三个基因(葡萄糖转运蛋白1、溶质载体家族16成员3和基本转录元件结合蛋白1)在发育和代谢中具有多种调节功能。TH似乎通过启动基因组或非基因组机制来诱导这些基因。令人惊讶的是,TH介导的成纤维细胞生长因子7和乙醇脱氢酶1B的下调在RTH患者的成纤维细胞中持续存在。这项对正常人类细胞中TH介导的基因表达的首次系统性研究确定了几个新的TH反应基因,并证明皮肤成纤维细胞适用于研究TH在健康和疾病中的作用。