Ohba Kenji, Leow Melvin Khee-Shing, Singh Brijesh Kumar, Sinha Rohit Anthony, Lesmana Ronny, Liao Xiao-Hui, Ghosh Sujoy, Refetoff Samuel, Sng Judy Chia Ghee, Yen Paul Michael
Cardiovascular and Metabolic Disorders Program (K.O., B.K.S., R.A.S., R.L., S.G., P.M.Y.), Duke-NUS Medical School, Singapore, Singapore 169857; Department of Endocrinology (M.K.-S.L.), Tan Tock Seng Hospital, Singapore, Singapore 229899; Singapore Institute for Clinical Sciences (M.K.-S.L.), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore 117609; Department of Physiology (R.L.), Universitas Padjadjaran, Bandung, West Java 45363, Indonesia; Departments of Medicine (X.-H.L., S.R.) and Pediatrics and Committee on Genetics (S.R.), The University of Chicago, Chicago, Illinois 60637; and Department of Pharmacology (J.C.G.S.), Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore 119228.
Endocrinology. 2016 Apr;157(4):1660-72. doi: 10.1210/en.2015-1848. Epub 2016 Feb 11.
Clinical symptoms may vary and not necessarily reflect serum thyroid hormone (TH) levels during acute and chronic hyperthyroidism as well as recovery from hyperthyroidism. We thus examined changes in hepatic gene expression and serum TH/TSH levels in adult male mice treated either with a single T3 (20 μg per 100 g body weight) injection (acute T3) or daily injections for 14 days (chronic T3) followed by 10 days of withdrawal. Gene expression arrays from livers harvested at these time points showed that among positively-regulated target genes, 320 were stimulated acutely and 429 chronically by T3. Surprisingly, only 69 of 680 genes (10.1%) were induced during both periods, suggesting desensitization of the majority of acutely stimulated target genes. About 90% of positively regulated target genes returned to baseline expression levels after 10 days of withdrawal; however, 67 of 680 (9.9%) did not return to baseline despite normalization of serum TH/TSH levels. Similar findings also were observed for negatively regulated target genes. Chromatin immunoprecipitation analysis of representative positively regulated target genes suggested that acetylation of H3K9/K14 was associated with acute stimulation, whereas trimethylation of H3K4 was associated with chronic stimulation. In an in vivo model of chronic intrahepatic hyperthyroidism since birth, adult male monocarboxylate transporter-8 knockout mice also demonstrated desensitization of most acutely stimulated target genes that were examined. In summary, we have identified transcriptional desensitization and incomplete recovery of gene expression during chronic hyperthyroidism and recovery. Our findings may be a potential reason for discordance between clinical symptoms and serum TH levels observed in these conditions.
在急性和慢性甲状腺功能亢进以及从甲状腺功能亢进恢复的过程中,临床症状可能会有所不同,不一定反映血清甲状腺激素(TH)水平。因此,我们研究了成年雄性小鼠在单次注射T3(每100克体重20微克)(急性T3)或每日注射14天(慢性T3)后再停药10天的情况下,肝脏基因表达和血清TH/TSH水平的变化。在这些时间点采集的肝脏基因表达阵列显示,在正向调节的靶基因中,有320个被T3急性刺激,429个被慢性刺激。令人惊讶的是,在680个基因中只有69个(10.1%)在两个时期都被诱导,这表明大多数急性刺激的靶基因发生了脱敏。约90%的正向调节靶基因在停药10天后恢复到基线表达水平;然而,680个基因中有67个(9.9%)尽管血清TH/TSH水平恢复正常,但并未恢复到基线水平。对于负向调节的靶基因也观察到了类似的结果。对代表性正向调节靶基因的染色质免疫沉淀分析表明,H3K9/K14的乙酰化与急性刺激有关,而H3K4的三甲基化与慢性刺激有关。在出生后慢性肝内甲状腺功能亢进的体内模型中研究发现,成年雄性单羧酸转运蛋白8基因敲除小鼠也表现出大多数被检测的急性刺激靶基因的脱敏现象。总之,我们已经确定了在慢性甲状腺功能亢进和恢复过程中存在转录脱敏和基因表达的不完全恢复。我们的发现可能是这些情况下临床症状与血清TH水平不一致的一个潜在原因。