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一年生鱼类贡氏假鳃鳉的卵子发生、卵黄蛋白原介导的卵巢退化及免疫反应

Oogenesis, vitellogenin-mediated ovarian degeneration and immune response in the annual fish Nothobranchius guentheri.

作者信息

Liu Tingting, Liu Shan, Ma Long, Li Fenglin, Zheng Zhaodi, Chai Rongfei, Hou Yanhan, Xie Yingbo, Li Guorong

机构信息

Shandong Provincial Key Laboratory of Animal Resistant Biology, School of Life Sciences, Shandong Normal University, 88 East Wenhua Road, Jinan 250014, Shandong, China.

Shandong Provincial Key Laboratory of Animal Resistant Biology, School of Life Sciences, Shandong Normal University, 88 East Wenhua Road, Jinan 250014, Shandong, China.

出版信息

Fish Shellfish Immunol. 2017 Jul;66:86-92. doi: 10.1016/j.fsi.2017.05.015. Epub 2017 May 4.

Abstract

Annual fishes of the genus Nothobranchius show expression of age-related biomarkers at behavioral and histological levels. They therefore represent an excellent animal model for aging studies. However, oocyte development, histological and biochemical degeneration and immune response of ovary in the annual fishes remain unclear. Here, using one of these short-lived fishes, Nothobranchius guentheri, we reported that oogenesis process was divided into four stages (oogonium, primary growth stage, cortical alveolus stage and vitellogenesis stage), and old ovaries showed histological degeneration (with decreased mature oocytes and increased atretic oocytes) accompaning with high levels of senescence-associated beta-galactosidase and lipofuscin by down-regulation of vitellogenin (the precursor of yolk proteins). Moreover, poly(I:C) induced inflammation with overexpression of NF-κB and IL-8, and up-regulated vitellogenin expression. It was a first analysis for vitellogenin to participate in ovarian degeneration and immune response in ovary of fish, indicating that vitellogenin fulfilled a critical role in ovary development and innate immune system.

摘要

诺氏鳉属的一年生鱼类在行为和组织学水平上表现出与年龄相关的生物标志物的表达。因此,它们是衰老研究的优秀动物模型。然而,一年生鱼类卵巢的卵母细胞发育、组织学和生化退化以及免疫反应仍不清楚。在这里,我们使用其中一种短命鱼类——贡氏假鳃鳉,报道了卵子发生过程分为四个阶段(卵原细胞、初级生长阶段、皮质泡阶段和卵黄发生阶段),并且老龄卵巢表现出组织学退化(成熟卵母细胞减少,闭锁卵母细胞增加),同时伴随着衰老相关β-半乳糖苷酶和脂褐素水平升高,这是由于卵黄蛋白原(卵黄蛋白的前体)表达下调所致。此外,聚肌苷酸-聚胞苷酸(poly(I:C))诱导炎症,伴有核因子κB(NF-κB)和白细胞介素-8(IL-8)的过表达,并上调卵黄蛋白原的表达。这是首次分析卵黄蛋白原参与鱼类卵巢退化和卵巢免疫反应,表明卵黄蛋白原在卵巢发育和先天免疫系统中发挥着关键作用。

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