Tonyushkina Ksenia N, Krug Stefanie, Ortiz-Toro Theresa, Mascari Tibor, Karlstrom Rolf O
Division of Pediatric Endocrinology, Baystate Children's Hospital, Baystate Health, Springfield, Massachusetts 01199.
Department of Biology, University of Massachusetts, Amherst, Massachusetts 01003.
Endocrinology. 2017 Sep 1;158(9):2774-2782. doi: 10.1210/en.2016-1935.
Low thyroid hormone (TH) conditions caused by a variety of prenatal and perinatal problems have been shown to alter postnatal regulatory thyrotropin (TSH) responsiveness to TH in humans and rodents. The mechanisms underlying this pituitary TH resistance remain unknown. Here we use the evolutionarily conserved zebrafish model to examine the effects of low TH on thyrotrope development and function. Zebrafish were exposed to the goitrogen 6-propyl-2-thiouracil (PTU) to block TH synthesis, and this led to an approximately 50% increase in thyrotrope numbers and an 8- to 10-fold increase in tshb mRNA abundance in 2-week-old larvae and 1-month-old juveniles. Thyrotrope numbers returned to normal 3 weeks after cessation of PTU treatment, demonstrating that these effects were reversible and revealing substantial plasticity in pituitary-thyroid axis regulation. Using a T4 challenge assay, we found that development under low-TH conditions did not affect the ability of T4 to suppress tshb mRNA levels despite the thyrotrope hyperplasia that resulted from temporary low-TH conditions. Together, these studies show that low developmental TH levels can lead to changes in thyrotrope number and function, providing a possible cellular mechanism underlying elevated TSH levels seen in neonates with either permanent or transient congenital hypothyroidism.
由各种产前和围产期问题导致的低甲状腺激素(TH)状况已被证明会改变人类和啮齿动物出生后促甲状腺激素(TSH)对TH的反应性。这种垂体TH抵抗的潜在机制仍然未知。在这里,我们使用进化上保守的斑马鱼模型来研究低TH对促甲状腺细胞发育和功能的影响。斑马鱼暴露于致甲状腺肿物质6-丙基-2-硫脲嘧啶(PTU)以阻断TH合成,这导致2周龄幼虫和1月龄幼鱼的促甲状腺细胞数量增加约50%,tshb mRNA丰度增加8至10倍。停止PTU治疗3周后,促甲状腺细胞数量恢复正常,表明这些影响是可逆的,并揭示了垂体-甲状腺轴调节中存在显著的可塑性。使用T4激发试验,我们发现尽管暂时的低TH状况导致促甲状腺细胞增生,但在低TH条件下发育并不影响T4抑制tshb mRNA水平的能力。总之,这些研究表明,发育过程中低TH水平可导致促甲状腺细胞数量和功能的变化,为患有永久性或暂时性先天性甲状腺功能减退症的新生儿中TSH水平升高提供了一种可能的细胞机制。