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OPA1缺乏在牛卵母细胞成熟过程中通过PINK1/帕金蛋白途径诱导线粒体自噬。

OPA1 deficiency induces mitophagy through PINK1/Parkin pathway during bovine oocytes maturation.

作者信息

Han Tiancang, Zhao Yuhan, Jiao Anhui, Sun Zhaoyang, Zhang Hongbo, Zhao Dazhuo, Wang Haijun, Gao Qingshan

机构信息

Engineering Research Center of North-East Cold Region Beef Cattle Science & Technology Innovation, Ministry of Education, Yanbian University, Yanji, 133002, China; Jilin Engineering Research Center of Yanbian Yellow Cattle Resources Reservation, China; Yanbian University, Yanji, 133002, China.

Yanbian Korean Nationality Autonomous Prefecture Animal Disease Prevention and Control Center, Yanji, 133002, China.

出版信息

Theriogenology. 2025 Mar 1;234:51-63. doi: 10.1016/j.theriogenology.2024.12.004. Epub 2024 Dec 4.

Abstract

In vitro embryo production (IVP) technology has been increasingly applied to beef cattle breeding. In vitro maturation (IVM) technology is the basis of IVP. However, the quality of in vitro-generated mature oocytes is still poor. Mitochondria are the energy factories of oocytes, so they are crucial for oocyte quality. OPA1 is a protein located on the mitochondrial inner membrane, and its main function is to mediate mitochondrial inner membrane fusion. This work demonstrated that OPA1 is expressed at different stages of meiosis in bovine oocytes. The inhibition of OPA1 activity resulted in a reduced rate of first polar body excretion from bovine oocytes and disruption of the spindle structure. OPA1 deficiency impacted mitochondria by leading to mitochondrial dysfunction, promoting mitochondrial fission, and inducing mitophagy through the PINK1/Parkin pathway. Taken together, our findings suggest that OPA1 is essential for bovine oocyte maturation and that OPA1 deficiency leads to mitochondrial dysfunction and promotes mitochondrial fission as well as mitophagy.

摘要

体外胚胎生产(IVP)技术已越来越多地应用于肉牛育种。体外成熟(IVM)技术是IVP的基础。然而,体外产生的成熟卵母细胞的质量仍然很差。线粒体是卵母细胞的能量工厂,因此它们对卵母细胞质量至关重要。OPA1是一种位于线粒体内膜上的蛋白质,其主要功能是介导线粒体内膜融合。这项工作表明,OPA1在牛卵母细胞减数分裂的不同阶段表达。OPA1活性的抑制导致牛卵母细胞第一极体排出率降低和纺锤体结构破坏。OPA1缺乏通过导致线粒体功能障碍、促进线粒体分裂以及通过PINK1/Parkin途径诱导线粒体自噬来影响线粒体。综上所述,我们的研究结果表明,OPA1对牛卵母细胞成熟至关重要,并且OPA1缺乏会导致线粒体功能障碍并促进线粒体分裂以及线粒体自噬。

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