Beyond the brain-Peripheral kisspeptin signaling is essential for promoting endometrial gland development and function

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作者：

Silvia León

Daniela Fernandois

Alexandra Sull

Judith Sull

Michele Calder

Kanako Hayashi

Moshmi Bhattacharya

Stephen Power

George A. Vilos

Angelos G. Vilos

Manuel Tena-Sempere

Andy V. Babwah

机构：

[1] Physiology & Immunology,Department of Cell Biology

[2] Faculty of Medicine and Instituto Maimonides de Investigacion Biomedica de Córdoba (IMIBIC)/Hospital Reina Sofia,Department of Physiology

[3] University of Córdoba,Department of Oncology

[4] Avda. Menéndez Pidal s/n,Department of Physiology

[5] The Children’s Health Research Institute,undefined

[6] Lawson Health Research Institute,undefined

[7] Department of Obstetrics and Gynaecology,undefined

[8] Division of Reproductive Endocrinology and Infertility,undefined

[9] Southern Illinois University School of Medicine,undefined

[10] Department of Physiology and Pharmacology,undefined

[11] London,undefined

[12] Ontario University of Western Ontario,undefined

[13] CIBEROBN,undefined

[14] Instituto de Salud Carlos III,undefined

[15] FiDiPro Program,undefined

[16] University of Turku,undefined

来源：

Scientific Reports | / 6卷

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摘要：

Uterine growth and endometrial gland formation (adenogenesis) and function, are essential for fertility and are controlled by estrogens and other regulators, whose nature and physiological relevance are yet to be elucidated. Kisspeptin, which signals via Kiss1r, is essential for fertility, primarily through its central control of the hypothalamic-pituitary-ovarian axis, but also likely through peripheral actions. Using genetically modified mice, we addressed the contributions of central and peripheral kisspeptin signaling in regulating uterine growth and adenogenesis. Global ablation of Kiss1 or Kiss1r dramatically suppressed uterine growth and almost fully prevented adenogenesis. However, while uterine growth was fully rescued by E2 treatment of Kiss1−/− mice and by genetic restoration of kisspeptin signaling in GnRH neurons in Kiss1r−/− mice, functional adenogenesis was only marginally restored. Thus, while uterine growth is largely dependent on ovarian E2-output via central kisspeptin signaling, peripheral kisspeptin signaling is indispensable for endometrial adenogenesis and function, essential aspects of reproductive competence.

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