题目：
HDAC3 maintains oocyte meiosis arrest by repressing amphiregulin expression before the LH surge
HDAC3通过抑制LH激增前的双向调节蛋白的表达来维持卵母细胞减数分裂的停止
句子翻译：
It is known that granulosa cells (GCs) mediate gonadotropin-induced oocyte meiosis resumption by releasing EGF-like factors in mammals, however, the detailed molecular mechanisms remain unclear. Here, we demonstrate that luteinizing hormone (LH) surgeinduced histone deacetylase 3 (HDAC3) downregulation in GCs is essential for oocyte maturation. Before the LH surge, HDAC3 is highly expressed in GCs. Transcription factors,such as FOXO1, mediate recruitment of HDAC3 to the amphiregulin (Areg) promoter, which suppresses AREG expression. With the LH surge, decreased HDAC3 in GCs enables histone H3K14 acetylation and binding of the SP1 transcription factor to the Areg promoter to initiate,AREG transcription and oocyte maturation. Conditional knockout of Hdac3 in granulosa cells in vivo or inhibition of HDAC3 activity in vitro promotes the maturation of oocytes independent of LH. Taking together, HDAC3 in GCs within ovarian follicles acts as a negative regulator of EGF-like growth factor expression before the LH surge.
摘要：已知颗粒细胞(GCs)通过释放EGF样因子介导促性腺激素诱导的卵母细胞减数分裂恢复，但具体的分子机制尚不清楚。在这里，我们证明了促黄体生成素(LH)过量诱导的GCs中组蛋白去乙酰化酶3(HDAC3)的下调对卵母细胞的成熟至关重要。在LH激增之前，HDAC3在GCs中高表达。转录因子，如FOXO1，介导HDAC3的募集到双向调节蛋白(Areg)启动子上，从而抑制AREG的表达。随着LH的激增，GCs中HDAC3的减少使组蛋白H3K14乙酰化，SP1转录因子与Areg启动子结合，启动AREG转录和卵母细胞成熟。体内条件敲除颗粒细胞中的Hdac3或体外抑制HDAC3活性可促进不依赖于LH的卵母细胞成熟。综上所述，在LH激增前，卵巢卵泡内GCs中的HDAC3作为EGF样生长因子表达的负调控因子。
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