Thyroid hormone regulated genes in the neonatal testis

An excess in thyroid hormone during rodent neonatal life causes abnormal prolifration and maturation of testicular cells, leading to reduced testis size and impairments in steroidogenesis, Sertoli cell function, spermatogenesis and fertility. The high expression of type 3 deiodinase in the neonatal testis protects this tissue from premature exposure to thyroid hormones, since this gene (Dio3) function is to degrade thyroid hormones. DIO3-deficient mice (Dio3KO) exhibit a marked reduction in Sertoli cell proliferation and testis size, abnormalities in the reproductive axis and impaired fertility (Martinez et al. 2016, Endocrinology157:1276). To identify genes that are untimely regulated by thyroid hormone in the developing testes, we have performed RNAseq in testis total RNA from wild type and DIO3KO mouse neonates. 8 samples were analyzed representing 2 experimental groups in biological cuadruplicates

啮齿类动物新生阶段甲状腺激素水平过高，会引发睾丸细胞异常增殖与成熟异常，最终导致睾丸体积缩小，同时损害类固醇生成（steroidogenesis）、支持细胞（Sertoli cell）功能、精子发生（spermatogenesis）与生育能力。新生小鼠睾丸中高表达的3型脱碘酶（type 3 deiodinase，Dio3）可保护该组织免受甲状腺激素的过早暴露，因为该基因的功能是降解甲状腺激素。DIO3缺陷小鼠（Dio3KO）会表现出支持细胞增殖能力下降、睾丸体积显著缩小、生殖轴异常以及生育能力受损的表型（Martinez等，2016，Endocrinology 157:1276）。为鉴定发育中睾丸内受甲状腺激素异常调控的基因，我们对野生型与DIO3KO新生小鼠的睾丸总RNA进行了RNA测序（RNAseq）。本研究共分析8个样本，涵盖2个实验组，每组设置4次生物学重复。