Connexin 43 (CX43) is a component of gap junctions. The lack of functional CX43 induces oxidative stress, autophagy, and apoptosis in somatic cells. However, the role of CX43 in the early development of porcine embryos is still unknown. Thus, the aim of this study was to investigate the role of CX43, and its underlying molecular mechanisms, on the developmental competence of early porcine embryos. We performed CX43 knockdown by microinjecting dsRNA into parthenogenetically activated porcine parthenotes. The blastocyst development rate and the total number of cells in the blastocysts were significantly reduced by CX43 knockdown. Results from FITC-dextran assays showed that CX43 knockdown significantly increased membrane permeability. ZO-1 protein was obliterated in CX43 knockdown blastocysts. Mitochondrial membrane potential and ATP production were significantly reduced following CX43 knockdown. Reactive oxygen species (ROS) levels were significantly increased in the CX43 knockdown group compared to those in control embryos. Moreover, CX43 knockdown induced autophagy and apoptosis. Our findings indicate that CX43 is essential for the development and preimplantation of porcine embryos and maintains mitochondrial function, cell junction structure, and cell homeostasis by regulating membrane permeability, ROS generation, autophagy, and apoptosis in early embryos.

中文翻译：

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连接蛋白 43 敲低诱导线粒体功能障碍并影响猪胚胎的早期发育能力

连接蛋白 43 (CX43) 是间隙连接的组成部分。功能性 CX43 的缺乏会在体细胞中诱导氧化应激、自噬和凋亡。然而，CX43在猪胚胎早期发育中的作用仍然未知。因此，本研究的目的是研究 CX43 及其潜在的分子机制对早期猪胚胎发育能力的作用。我们表演了CX43通过将 dsRNA 显微注射到孤雌生殖激活的猪孤雌生殖中来进行敲低。囊胚发育率和囊胚中的细胞总数显着降低CX43击倒。FITC-葡聚糖测定的结果表明，CX43敲低显着增加膜通透性。ZO-1 蛋白在CX43击倒囊胚。线粒体膜电位和 ATP 产生显着降低后CX43击倒。活性氧（ROS）水平显着增加CX43与对照胚胎中的相比，敲低组。而且，CX43敲低诱导自噬和细胞凋亡。我们的研究结果表明CX43对猪胚胎的发育和植入前至关重要，并通过调节早期胚胎的膜通透性、活性氧生成、自噬和细胞凋亡来维持线粒体功能、细胞连接结构和细胞稳态。