The kisspeptin/KISS1R signaling system: Beyond the brain

繁殖是一个生物学过程，通过这个过程， 有机体自我繁殖，这是所有已知生命的基本特征.通过 了解调节生殖的因素我们可以提高 重要的家养和野生动植物品种繁育计划。同样， 通过干预，我们可以制定新的战略来减少人口 对脆弱的生态系统构成威胁并导致 母猫和母狗的不孕不育是全球努力的一部分，以规范 野生动物和宠物的数量。旨在监管的战略 繁殖通常以大脑为目标，以增加或减少可用性 一种名为促性腺激素释放激素(GnRH)的激素。GnRH也是 被称为繁殖的主要调节者，负责生产 卵子和精子。当卵子与精子受精时，它会发育成 胚胎附着在子宫壁上并发育成 胎儿。依附过程被称为植入，这是一个关键的 成功怀孕的限速步骤。 最近，我们发现 Kispeptin(KP)和KISS1R这两种蛋白质是 发现于小鼠的子宫中，似乎是成功胚胎所必需的 植入。然而，在我们可以自信地说，KP和KISS1R 调控胚胎在子宫内的植入还需要更多的研究。vt.给出 它们潜在的生物学功能，进行这些研究是很重要的 了解Kp和KISS1R是如何调控着床和生殖的。 为此，我们将创造一种缺乏产生Kp和Kp的能力的老鼠 KISS1R在它的子宫中，然后问这对 胚胎植入。如果胚胎不能植入，这将是无可辩驳的 Kp和KISS1R调控着床的证据。如果我们做出这些观察 然后我们将询问是什么调节子宫中的KP和KISS1R水平。在这里我们 将重点放在性类固醇、雌激素(E)和孕激素(P)上。E和P是 是由卵巢制造的，对胚胎植入和存活至关重要。 因此，卵巢E和/或P可能调节子宫KP和KISS1R 级别。在老鼠身上，我们切除了卵巢，从而去除了体内的 E和P的来源，我们将添加回E和P，并确定这会产生什么影响 在Kp和KISS1R水平上。如果我们发现Kp和KISS1R水平是 我们将得出结论，子宫KP和KISS1R是由E2和P4调节的 蛋白质。 了解是什么调节Kp和KISS1R水平，以及Kp和KISS1R KISS1R反过来进行调控，是靶向KP和 KISS1R在子宫中，以促进或抑制着床，从而 繁殖。

Reproduction is a biological process by which an organism propagates itself and it a fundamental feature of all known life. By understanding the factors that regulate reproduction we can enhance the breeding programs of important domestic and wildlife species. Similarly, through intervention we can develop novel strategies to reduce the population of wildlife species that pose a threat to fragile ecosystems and induce sterility among female cats and dogs as part of a global effort to regulate the population of both feral animals and pets. Strategies aimed at regulating reproduction often target the brain, to increase or decrease the availability of a hormone called the gonadotropin-releasing hormone (GnRH). GnRH is also called the master regulator of reproduction and is responsible for the production of the egg and sperm. When an egg is fertilized by a sperm it develops into an embryo which attaches itself to the wall of the uterus and develops into the fetus. The attachment process is called implantation and it is a critical rate-limiting step in achieving a successful pregnancy. Recently, we discovered that two proteins, kisspeptin (KP) and the kisspeptin receptor (KISS1R), are found in the uterus of mice and appear necessary for successful embryo implantation. However, before we can confidently say that KP and KISS1R regulate embryo implantation in the uterus more studies are required. Given their potential biological function, it is important to conduct these studies to understand how KP and KISS1R regulate implantation and thereby reproduction. To do this, we will create a mouse that lacks the ability to produce KP and KISS1R in its uterus and then ask what effect this has on the ability of the embryo to implant. If the embryo fails to implant this will be irrefutable proof that KP and KISS1R regulate implantation. If we make those observations we will then ask what regulates KP and KISS1R levels in the uterus. Here we will focus on the sex steroids, estrogen (E) and progesterone (P). E and P are made by the ovaries and are critical for embryo implantation and survival. Thus, it is possible that ovarian E and/or P regulate uterine KP and KISS1R levels. Using mice in which we have removed the ovaries and hence the internal source of E and P, we will add back E and P and determine what effect this has on the levels of KP and KISS1R. If we find that KP and KISS1R levels are altered we will conclude that uterine KP and KISS1R are E2- and P4-regulated proteins. Understanding what regulates KP and KISS1R levels and what KP and KISS1R regulate in turn, are the first critical steps towards targeting KP and KISS1R in the uterus in order to enhance or inhibit implantation and thereby reproduction.