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研究表明颗粒细胞凋亡是卵泡闭锁的重要原因,调控颗粒细胞凋亡的因素是多种的,而生殖激素如生长激素、抑制素、活化素、卵泡抑素等间接地和直接地对卵巢卵泡颗粒细胞凋亡发挥重要的综合调控作用,这些激素通过多种信号转导途径调节颗粒细胞的凋亡,成为卵泡的存活因子和死亡因子.这些途径相互交联,构成信号网络,与卵巢的旁分泌、内分泌、自分泌途径一起参与卵泡闭锁和颗粒细胞的凋亡. 相似文献
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卵巢是家禽的重要繁殖器官,会产生大量卵泡,而卵泡在生长发育的各个阶段中都可能因为不同因素的调控而发生闭锁,最终导致繁殖性能衰退。颗粒细胞对卵泡的生长发育有重要调控作用,其凋亡会诱导卵泡发生闭锁。诱导颗粒细胞发生凋亡的因素较多,包括激素、细胞因子、氧化应激、线粒体及其他体外因素。颗粒细胞凋亡主要由线粒体途径导致,其涉及到半胱天冬酶（Caspase）家族参与,当线粒体裂解时会释放细胞色素C （Cyt-C）,随后形成凋亡小体激活Caspase-3和Caspase-8,最终激活Caspase-9导致颗粒细胞凋亡;当颗粒细胞发生凋亡,家禽体内卵泡丧失生物功能并且卵泡细胞之间的调控失衡,促使卵泡内卵母细胞和膜细胞凋亡,最终导致卵泡发生闭锁;颗粒细胞在存活状态下所分泌的生长因子、性腺类固醇、细胞因子能减少卵母细胞氧化损伤,防止细胞内活性氧（ROS）水平过高导致的线粒体DNA损伤,从而避免线粒体功能障碍而造成的颗粒细胞凋亡。作者从颗粒细胞凋亡及其影响因素、颗粒细胞凋亡和卵泡闭锁的关系、颗粒细胞凋亡对卵泡闭锁的影响3个方面进行阐述,以期为减少卵泡闭锁、提高家禽繁殖性能提供理论依据。 相似文献
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微小核糖核酸(microRNA,miRNA)是一类内源性非编码RNA,具有广泛的基因表达调控作用,可以在转录后水平通过影响靶基因来调控相应蛋白质的表达,进而调节细胞的生命活动。miRNA在哺乳动物卵泡颗粒细胞中表达,并调控颗粒细胞的凋亡。颗粒细胞作为卵巢卵泡中数量最多的细胞群,在卵泡发育过程中起着至关重要的作用,不仅为卵母细胞提供营养物质,还调控其发育和成熟。颗粒细胞凋亡是导致卵泡闭锁的重要原因,影响卵泡的数量和质量从而影响雌性动物的繁殖性能。颗粒细胞凋亡过程受多种因素的调控。文章简述了miRNA对卵巢颗粒细胞凋亡的调控作用及其机制,其中包括miRNA通过调控激素分泌和细胞凋亡相关因子的表达进而调节颗粒细胞的凋亡,miRNA对颗粒细胞凋亡相关信号通路的影响,miRNA调控颗粒细胞凋亡导致的卵巢相关疾病,并总结了对颗粒细胞凋亡有调控作用的miRNA,以及miRNA在疾病诊断和治疗中的潜在作用,以期为后续相关卵巢疾病的发病机制和治疗方案研究,以及提高雌性哺乳动物生殖性能提供指导和参考。 相似文献
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《畜牧兽医学报》2015,(6)
为了探明促卵泡素(Follicle stimulating hormone,FSH)和促黄体素(Luteinizing hormone,LH)对体外培养的牦牛卵泡颗粒细胞凋亡及甾体激素分泌的影响,揭示促性腺激素调控卵泡发育的机理,采用细胞培养和显微观察技术,建立了牦牛卵泡颗粒细胞体外培养体系,观察分析牦牛卵泡颗粒细胞体外培养的生长特征和凋亡的形态特征;采用流式细胞技术(Flow cytometry,FCM)和放射免疫测定技术(Radioimmunoassay,RIA),分析了添加不同浓度的FSH和LH对牦牛卵泡颗粒细胞凋亡和雌二醇(Estradiol,E2)、孕酮(Progesterone,P)分泌的影响。结果显示,体外培养的牦牛卵泡颗粒细胞呈现出典型的上皮样细胞生长特性,具有典型的"S"形生长曲线,体外培养的牦牛颗粒细胞偶尔可见细胞核浓缩、边集化、染色质固缩、内质网疏松等凋亡的形态特征。在添加0.050~5.000IU·mL-1FSH,随着浓度的增加,凋亡细胞比例逐渐降低,E2和P水平呈上升趋势;在添加浓度达到5.000IU·mL-1时,凋亡细胞比例最低降到7.3%,与对照组差异极显著(P0.01)。低浓度的LH(0.050~0.500IU·mL-1),可以抑制颗粒细胞凋亡,促使E2和P分泌增加;高浓度的LH(5.000IU·mL-1)则促使颗粒细胞凋亡,对颗粒细胞分泌E2和P的影响不明显。这一结果表明,FSH和LH可通过调节牦牛颗粒细胞的凋亡及分泌功能,在调控卵泡发育及排卵的过程中发挥重要作用。 相似文献
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为探讨孕马血清促性腺激素（PMSG）对2－3月龄性未成熟的小母猪卵巢中卵泡发育，卵泡闭锁以及卵泡颗粒细胞凋亡的影响，就其注射PMSG后24，48，72，96h卵巢中各类卵泡数量，颗粒细胞凋亡比例及外周血浆中类固醇激素水平等进行了研究。结果如下：（1）未注射PMSG前，性未成熟小母猪卵巢表面卵泡总数（10．5个／卵巢）及各类卵泡数（小卵泡9个／卵巢，中等卵泡数1．5个／卵巢）均较少；注射PMSG后24h，小卵泡数（24个／卵巢），中等卵泡数（6．5个／卵巢）和大卵泡数（1．5个／卵巢）与对照组相比均明显增多；至注射PMSG后96h，小卵泡（4．5个／卵巢）和中等卵泡数（1．5个／卵巢）均明显减少，但大卵泡数量仍较多（4．5个／卵巢）。（2）未注射PMSG前，性未成熟小母猪中类卵泡中的颗粒细胞凋亡比例均较高，小卵泡和中等卵泡分别为24．8％和34．4％；注射PMSG事24h，颗粒细胞凋亡比例显著降低（P＜0．05），小卵泡和中等卵泡分别为10．7％和13．7％，至PMSG事72h，小卵泡和中等卵泡的颗粒细胞凋亡比例开始显著升高（P＜0．05），而大卵泡在出现后颗粒细胞凋亡比例较低且无较大波动。（2）在未注射PMSG前，血清中的雌二醇含量仅为15．3ng/L，孕酮则由于含量大低而未能检测到；在注射PMSG后，雌二醇和孕酮水平均升高，雌二醇在注射PMSG后72h时达最高值59.2ng/L，孕酮在注射PMSG后48h出现最高值1.7 μg/L。以上结果表明，在性未成熟的2－3月龄小母猪，卵泡颗粒细胞凋亡比例很高，导致卵巢表面各类卵泡数量均较少，血清类固醇激素水平也很低，而PMSG可在其尚未建立起自身下丘脑－垂体－性腺轴的激素调节机制情况,显著抑制颗粒细胞亡，从而抑制卵泡的闭锁，促进卵泡的发育，并进而提高血清中类固醇激素的水平。 相似文献
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为了研究八眉猪卵泡闭锁过程中卵泡颗粒细胞的凋亡情况、卵泡组织结构变化以及卵泡膜内层毛细血管变化特点,试验在体视显微镜下观察并将卵泡分为健康卵泡、早期闭锁卵泡和晚期闭锁卵泡,用Hoechst 33258对闭锁不同时期卵泡颗粒细胞凋亡情况进行检测。采用苏木精-伊红(H.E.)染色法对卵泡膜层组织结构进行观察,CD34免疫组化染色对卵泡膜上毛细血管的分布进行观察。结果表明:随着卵泡闭锁程度的加深,卵泡颗粒细胞逐渐脱落进入卵泡腔,颗粒细胞凋亡增多,分布在卵泡膜内层的毛细血管随着卵泡闭锁程度的加深逐渐消失。说明卵泡颗粒细胞凋亡和卵泡膜上微血管消失是八眉猪卵泡闭锁的重要特征。 相似文献
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本试验采用TUNEL原位法和DNA梯度电泳法等方法对卵巢上闭锁卵泡中凋亡的颗粒细胞类型和分布状况等进行研究。结果表明，辽宁绒山羊闭锁卵泡是细胞凋亡引起的。DNA梯状电泳表明，不同健康程度卵泡颗粒细胞凋亡程度不同；而颗粒细胞TUNEL原位标记表明，健康卵泡、轻度闭锁卵泡及闭锁卵泡中颗粒细胞凋亡比例分别为13.21%±1.23％、32.13%±2.13％、51.31%±3.02％；不同健康程度卵泡中类固醇激素水平不同，健康卵泡中E2水平较高，孕酮浓度较低；闭锁卵泡中E2浓度较低，P4浓度较高，健康、轻度闭锁和闭锁三类卵泡中E2/P4比值分别是2.62±0.03、0.074±0.0003、0.028±0.0004。 相似文献
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家禽衰老进程中卵泡发生快速闭锁,这种生物学现象很可能是导致家禽后期产蛋性能下降的重要原因。卵泡微环境影响颗粒细胞与卵母细胞的互作关系,并决定着卵泡的生长与成熟。研究表明,颗粒细胞凋亡的发生是引起卵泡闭锁发生的主要因素。本文综述了近年来衰老进程中颗粒细胞微环境变化及卵泡闭锁信号相关研究,主要包括激素紊乱、氧化应激等因素,同时本文深入讨论氧化应激诱导的线粒体损伤和内质网应激现象,旨在阐释衰老诱导的颗粒细胞微环境变化与卵泡闭锁机制,为产蛋后期蛋禽繁殖性能或产蛋性能的调控提供参考。 相似文献
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Matsuda-Minehata F Inoue N Goto Y Manabe N 《The Journal of reproduction and development》2006,52(6):695-705
In the mammalian ovary, follicular development and atresia are closely regulated by cell death and survival-promoting factors, including hormones (gonadotropins) and intraovarian regulators (gonadal steroids, cytokines, and intracellular proteins). Several hundred thousand primordial follicles are present in the mammalian ovary; however, only a limited number of primordial follicles develop to the preovulatory stage and ovulate. The others, more than 99% of follicles, will be eliminated via a degenerative process known as "atresia". The endocrinological regulatory mechanisms involved in follicular development and atresia have been characterized to a large extent, but the precise temporal and molecular mechanisms involved in the regulation of these events have remained largely unknown. Recent studies suggest that the apoptosis of ovarian granulosa cells plays a major role in follicular atresia. In this review, we provide an overview of development and atresia of follicles, and apoptosis of granulosa cells in mammals. 相似文献
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The mammalian ovary is an extremely dynamic organ in which a large majority of follicles are effectively eliminated throughout their reproductive life. Due to the numerous efforts of researchers, mechanisms regulating follicular growth and atresia in mammalian ovaries have been clarified, not only their systemic regulation by hormones (gonadotropins) but also their intraovarian regulation by gonadal steroids, growth factors, cytokines and intracellular proteins. Granulosa cells in particular have been demonstrated to play a major role in deciding the fate of follicles, serving molecules that are essential for follicular growth and maintenance as well as killing themselves by an apoptotic process that results in follicular atresia. In this review, we discuss the factors that govern follicular growth and atresia, with a special focus on their regulation by granulosa cells. First, ovarian folliculogenesis in adult life is outlined. Then, we explain about the regulation of follicular growth and atresia by granulosa cells, in which hormones, growth factors and cytokines, death ligand-receptor system and B cell lymphoma/leukemia 2 (BCL2) family members (mitochondria-mediated apoptosis) are further discussed. 相似文献
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Recent studies suggest that ovarian follicular atresia is associated with DNA fragmentation and degeneration of granulosa cells, the hallmark of programmed cell death or apoptosis. Apoptosis of granulosa cells play a major role in follicular atresia. These studies have also demonstrated the involvement of tumour suppressors, apoptotic proteins and survival factors. These factors contribute to the developmental decision as to whether the ovarian follicles mature or undergo atresia. However, the precise temporal and molecular events involved in the apoptotic pathways in this process need to be elucidated. The present report summarizes the role of Jun N‐terminal kinase (JNK), p38 mitogen activated protein kinase (p38 MAPK), and extracellular‐signal regulated kinase (ERK)‐signalling module in the regulation of pro‐ and anti‐apoptotic factors of the granulosa cells in regulating follicular atresia. The findings presented here suggest that the loss of tropic hormone support is translated into the attenuation of Raf‐1‐MAPK/ERK kinase (MEK)‐ERK‐signalling pathway of the granulosa cells and this results in the decreased phosphorylation of the pro‐apoptotic BAD. 相似文献
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Contents In this experiment, the possibility that the follicular-wall cells' death during ovarian follicular atresia occurs as a result of apoptosis was examined. Programmed cell death or apoptosis is a process whereby cells die in a controlled fashion, triggered by changes in levels of specific physiological stimuli. Morphological transformations of the cells are preceded by endo- nuclease-mediated genomic-DNA cleavage. The analysis of DNA from the theca and granulosa layers of follicles indicated that internucleosomal fragmentation of DNA occurred in atretic granulosa cells but not in atretic theca cells. The healthy granulosa and theca cells in all classes of follicles showed no apoptosis. This paper demonstrates that the death of porcine ovarian-follicle walls can be caused by different processes and, contrary to granulosa cells' apoptosis, either does not or only partly concerns the internal theca layer. 相似文献
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