Using RT‑qPCR and immunofluorescence, we determined that NR0B1 was mainly expressed in mouse SCs in an age-dependent manner from 2-8 weeks of age postnatally. In the present study, we have identified NR0B1 as a novel AR co-repressor in mouse SCs. As the association between NR0B1 and AR remains unclear in mouse SCs, we decided to further explore the relationship between them.
Many genes are directly regulated by androgen and its AR, which are involved in spermatogenesis and male infertility.
Testicular androgen receptor (AR) was also expressed in SCs. The transgenic expression of Nr0b1 under the control of the Müllerian-inhibiting substance promoter (MIS-Nr0b1), which is selectively expressed in SCs, improves fertility. The targeted mutagenesis of Nr0b1 in mice has revealed a primary gonadal defect characterized by the overexpression of aromatase and cellular obstruction of the seminiferous tubules and efferent ductules, leading to germ cell death and infertility. Mutations of NR0B1 in humans cause adrenal failure and hypogonadotropic hypogonadism. Nuclear receptor subfamily 0 group B member 1 (Nr0b1) is an atypical member of the nuclear receptor family that is predominantly expressed in mouse Sertoli cells (SCs).
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