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Selective Regulation of Oocyte Meiotic Events Enhances Progress in Fertility Preservation Methods

機(jī)譯：卵母細(xì)胞減數(shù)分裂事件的選擇性調(diào)節(jié)提高了生育力保存方法的進(jìn)展

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Following early embryonic germ cell migration, oocytes are surrounded by somatic cells and remain arrested at diplotene stage until luteinizing hormone (LH) surge. Strict regulation of both meiotic arrest and meiotic resumption during dormant stage are critical for future fertility. Inter-cellular signaling system between the somatic compartment and oocyte regulates these meiotic events and determines the follicle quality. As well as the collected number of eggs, their qualities are also important for in vitro fertilization (IVF) outcome. In spontaneous and IVF cycles, germinal vesicle (GV)–stage oocytes, premature GV breakdown, and persistence of first meiotic arrest limit the reproductive performance. Likewise, both women with premature ovarian aging and young cancer women are undergoing chemoradiotherapy under the risk of follicle loss because of unregulated meiotic events. Understanding of oocyte meiotic events is therefore critical for the prevention of functional ovarian reserve. High levels of cyclic guanosine monophophate (cGMP), cyclic adenosine monophophate (cAMP) and low phosphodiesterase (PDE) 3A enzyme activity inside the oocyte are responsible for maintaining of meiotic arrest before the LH surge. cGMP is produced in the somatic compartment, and natriuretic peptide precursor C (Nppc) and natriuretic peptide receptor 2 (Npr2) regulate its production. cGMP diffuses into the oocyte and reduces the PDE3A activity, which inhibits the conversion of cAMP to the 5′AMP, and cAMP levels are enhanced. In addition, oocyte itself has the ability to produce cAMP. Taken together, accumulation of cAMP inside the oocyte induces protein kinase activity, which leads to the inhibition of maturation-promoting factor and meiotic arrest also continues. By stimulating the expression of epidermal growth factor, LH inhibits the Nppc/Npr2 system, blocks cGMP synthesis, and initiates meiotic resumption. Oocytes lacking the functional of this pathway may lead to persistence of the GV oocyte, which reduces the number of good quality eggs. Selective regulation of somatic cell signals and oocyte meiotic events enhance progress in fertility preservation methods, which may give us the opportunity to prevent follicle loss in prematurely aging women and young women with cancer are undergoing chemoradiotherapy.
機(jī)譯：在早期胚胎生殖細(xì)胞遷移后，卵母細(xì)胞被體細(xì)胞包圍，并停留在二倍體階段，直到促黃體生成激素（LH）激增。休眠期中減數(shù)分裂停滯和減數(shù)分裂恢復(fù)的嚴(yán)格調(diào)節(jié)對于未來的生育能力至關(guān)重要。體細(xì)胞室和卵母細(xì)胞之間的細(xì)胞間信號系統(tǒng)調(diào)節(jié)這些減數(shù)分裂事件并確定卵泡質(zhì)量。除了收集到的卵子數(shù)量外，卵子的質(zhì)量對于體外受精（IVF）結(jié)果也很重要。在自發(fā)和IVF周期中，生小泡（GV）期卵母細(xì)胞，GV過早分解和第一次減數(shù)分裂停滯的持續(xù)存在限制了繁殖性能。同樣，卵巢早衰的婦女和年輕的癌癥婦女由于減數(shù)分裂事件的失控而正在接受濾泡治療，處于卵泡丟失的風(fēng)險中。因此，了解卵母細(xì)胞減數(shù)分裂事件對于預(yù)防功能性卵巢儲備至關(guān)重要。卵母細(xì)胞內(nèi)部高水平的環(huán)鳥苷單磷酸酯（cGMP），環(huán)腺苷單磷酸酯（cAMP）和低磷酸二酯酶（PDE）3A酶活性是維持LH激增之前減數(shù)分裂停滯的原因。 cGMP在體細(xì)胞室中產(chǎn)生，利鈉肽前體C（Nppc）和利鈉肽受體2（Npr2）調(diào)節(jié)其產(chǎn)生。 cGMP擴(kuò)散進(jìn)入卵母細(xì)胞并降低PDE3A活性，從而抑制了cAMP向5'AMP的轉(zhuǎn)化，并提高了cAMP水平。另外，卵母細(xì)胞本身具有產(chǎn)生cAMP的能力。綜上所述，卵母細(xì)胞內(nèi)cAMP的積累會誘導(dǎo)蛋白激酶活性，從而抑制成熟促進(jìn)因子，減數(shù)分裂停滯也將繼續(xù)。通過刺激表皮生長因子的表達(dá)，LH抑制Nppc / Npr2系統(tǒng)，阻斷cGMP合成，并開始減數(shù)分裂恢復(fù)。缺乏該途徑功能的卵母細(xì)胞可能導(dǎo)致GV卵母細(xì)胞持續(xù)存在，從而降低了優(yōu)質(zhì)卵的數(shù)量。體細(xì)胞信號和卵母細(xì)胞減數(shù)分裂事件的選擇性調(diào)節(jié)提高了生育力保存方法的進(jìn)展，這可能使我們有機(jī)會預(yù)防正在接受化學(xué)放療的早衰婦女和年輕婦女的卵泡丟失。

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