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胎儿鼠脑中 kiss1 和 kiss1r 的发育特征和性别二态性表达。

Developmental profile and sexually dimorphic expression of kiss1 and kiss1r in the fetal mouse brain.

机构信息

Oregon Health and Science University , Portland, OR , USA.

出版信息

Front Endocrinol (Lausanne). 2013 Oct 11;4:140. doi: 10.3389/fendo.2013.00140. eCollection 2013.

DOI:10.3389/fendo.2013.00140
PMID:24130552
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3795359/
Abstract

The hypothalamic-pituitary-gonadal axis (HPG) is a complex neuroendocrine circuit involving multiple levels of regulation. Kisspeptin neurons play essential roles in controlling the HPG axis from the perspectives of puberty onset, oscillations of gonadotropin releasing hormone (GnRH) neuron activity, and the pre-ovulatory LH surge. The current studies focus on the expression of kisspeptin during murine fetal development using in situ hybridization (ISH), quantitative reverse transcription real-time PCR (QPCR), and immunocytochemistry. Expression of mRNA coding for kisspeptin (KISS1) and its receptor KISS1R was observed at embryonic (E) day 13 by ISH. At E13 and other later ages examined, Kiss1 signal in individual cells within the arcuate nucleus (ARC) appeared stronger in females than males. ISH examination of agonadal steroidogenic factor-1 (Sf1) knockout mice revealed that E17 XY knockouts (KO) resembled wild-type (WT) XX females. These findings raise the possibility that gonadal hormones modulate the expression of Kiss1 in the ARC prior to birth. The sex and genotype differences were tested quantitatively by QPCR experiments in dissected hypothalami from mice at E17 and adulthood. Females had significantly more Kiss1 than males at both ages, even though the number of cells detected by ISH was similar. In addition, QPCR revealed a significant difference in the amount of Kiss1 mRNA in Sf1 mice with WT XY mice expressing less than XY KO and XX mice of both genotypes. The detection of immunoreactive KISS1 in perikarya of the ARC at E17 indicates that early mRNA is translated to peptide. The functional significance of this early expression of Kiss1 awaits elucidation.

摘要

下丘脑-垂体-性腺轴(HPG)是一个涉及多个调节水平的复杂神经内分泌回路。 kisspeptin 神经元在控制 HPG 轴方面发挥着重要作用,从青春期开始、促性腺激素释放激素(GnRH)神经元活动的波动以及促黄体生成素(LH)的预排卵激增等方面。目前的研究集中在使用原位杂交(ISH)、定量逆转录实时 PCR(QPCR)和免疫细胞化学技术研究 kisspeptin 在小鼠胎儿发育过程中的表达。通过 ISH 观察到编码 kisspeptin(KISS1)及其受体 KISS1R 的 mRNA 在胚胎(E)天 13 时表达。在 E13 天和其他后期检查中,在弓状核(ARC)内的单个细胞中,Kiss1 信号在雌性中比雄性中更强。对去势类固醇生成因子-1(Sf1)敲除小鼠的 ISH 检查显示,E17 XY 敲除(KO)类似于野生型(WT)XX 雌性。这些发现提出了一种可能性,即在出生前,性腺激素调节 ARC 中 Kiss1 的表达。通过在 E17 天和成年期从小鼠分离的下丘脑进行 QPCR 实验,对性别和基因型差异进行了定量测试。在这两个年龄段,雌性的 Kiss1 都明显多于雄性,尽管通过 ISH 检测到的细胞数量相似。此外,QPCR 显示 Sf1 小鼠中 Kiss1 mRNA 的量存在显着差异,其中 WT XY 小鼠的表达少于 XY KO 和两种基因型的 XX 小鼠。在 E17 时 ARC 神经元中检测到免疫反应性 KISS1,表明早期 mRNA 被翻译为肽。这种 Kiss1 早期表达的功能意义尚待阐明。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/a9356ec8d67a/fendo-04-00140-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/ceb1728213b7/fendo-04-00140-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/72cc6debc8b0/fendo-04-00140-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/6dfd2f1cfef1/fendo-04-00140-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/0b062a1917b2/fendo-04-00140-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/e6e052947de6/fendo-04-00140-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/044a11c3ebe3/fendo-04-00140-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/a9356ec8d67a/fendo-04-00140-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/ceb1728213b7/fendo-04-00140-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/72cc6debc8b0/fendo-04-00140-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/6dfd2f1cfef1/fendo-04-00140-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/0b062a1917b2/fendo-04-00140-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/e6e052947de6/fendo-04-00140-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/044a11c3ebe3/fendo-04-00140-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d40/3795359/a9356ec8d67a/fendo-04-00140-g007.jpg

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