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GnRH Receptor Expression and Reproductive Function Depend on JUN in GnRH Receptor‒Expressing Cells

机译：GnRH受体表达细胞中GnRH受体的表达和生殖功能取决于JUN

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摘要

Gonadotropin-releasing hormone (GnRH) from the hypothalamus regulates synthesis and secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary gonadotropes. LH and FSH are heterodimers composed of a common α-subunit and unique β-subunits, which provide biological specificity and are limiting components of mature hormone synthesis. Gonadotrope cells respond to GnRH via specific expression of the GnRH receptor (Gnrhr). GnRH induces the expression of gonadotropin genes and of the Gnrhr by activation of specific transcription factors. The JUN (c-Jun) transcription factor binds to AP-1 sites in the promoters of target genes and mediates induction of the FSHβ gene and of the Gnrhr in gonadotrope-derived cell lines. To analyze the role of JUN in reproductive function in vivo, we generated a mouse model that lacks JUN specifically in GnRH receptor‒expressing cells (conditional JUN knockout; JUN-cKO). JUN-cKO mice displayed profound reproductive anomalies such as reduced LH levels resulting in lower gonadal steroid levels, longer estrous cycles in females, and diminished sperm numbers in males. Unexpectedly, FSH levels were unchanged in these animals, whereas Gnrhr expression in the pituitary was reduced. Steroidogenic enzyme expression was reduced in the gonads of JUN-cKO mice, likely as a consequence of reduced LH levels. GnRH receptor‒driven Cre activity was detected in the hypothalamus but not in the GnRH neuron. Female, but not male, JUN-cKO mice exhibited reduced GnRH expression. Taken together, our results demonstrate that GnRH receptor‒expression levels depend on JUN and are critical for reproductive function.
机译：下丘脑的促性腺激素释放激素（GnRH）调节垂体前叶促性腺激素的促黄体生成激素（LH）和促卵泡激素（FSH）的合成和分泌。 LH和FSH是由共同的α亚基和独特的β亚基组成的异二聚体，它们提供生物学特异性，并且是成熟激素合成的限制性成分。促性腺激素细胞通过GnRH受体（Gnrhr）的特异性表达来响应GnRH。 GnRH通过激活特定转录因子诱导促性腺激素基因和Gnrhr的表达。 JUN（c-Jun）转录因子与靶基因启动子中的AP-1位点结合，并介导促性腺激素衍生细胞系中FSHβ基因和Gnrhr的诱导。为了分析JUN在体内生殖功能中的作用，我们建立了一个小鼠模型，该模型在GnRH受体表达细胞（条件性JUN敲除； JUN-cKO）中缺少JUN。 JUN-cKO小鼠表现出深刻的生殖异常，例如LH水平降低，导致性腺激素水平降低，雌性发情周期延长，雄性精子数量减少。出乎意料的是，这些动物的FSH水平没有变化，而垂体中Gnrhr的表达却降低了。在JUN-cKO小鼠的性腺中，类固醇生成酶的表达降低，这可能是LH水平降低的结果。在下丘脑中检测到GnRH受体驱动的Cre活性，但在GnRH神经元中未检测到。雌性而非雄性JUN-cKO小鼠表现出降低的GnRH表达。两者合计，我们的结果表明，GnRH受体表达水平取决于JUN，对生殖功能至关重要。

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