IGF-1通过激活Wnt/β-catenin通路促进猪胚胎滋养外胚层细胞增殖。

IF 8.2 2区 生物学 Q1 CELL BIOLOGY
Min Ju Kim, Hyo-Gu Kang, Se-Been Jeon, Ji Hyeon Yun, Eun Young Choi, Pil-Soo Jeong, Bong-Seok Song, Sun-Uk Kim, Seong-Keun Cho, Bo-Woong Sim
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引用次数: 0

摘要

背景:胰岛素样生长因子1 (IGF-1)影响胚胎发生的各个方面,包括胚胎发育。本研究研究了IGF-1对猪胚胎早期胚胎发育的影响,重点研究了其与Wnt/β-catenin信号通路的相互作用,Wnt/β-catenin信号通路是细胞粘附和增殖的关键调节因子。方法:利用猪胚胎进行化学处理实验,研究囊胚发育及其机制。进行细胞凋亡、免疫化学、基因表达、蛋白定量分析,差异均有统计学意义。结果:在胚胎发育的早期阶段,IGF-1治疗显著提高了发育参数,特别是囊胚形成率。有趣的是,IGF-1增加了滋养外胚层(TE)细胞的增殖。TE是囊胚的重要组成部分,维持其结构。猪胚胎的成功发育依赖于TE的正确形成和功能。IGF-1上调TE分化和紧密连接相关功能蛋白的表达。值得注意的是,与胚胎发育的前3天(0-3天)相比,在胚胎发育的最后3天(3-6天)进行IGF-1治疗时,这些效果更为明显。此外,我们发现IGF-1促进Wnt/β-catenin信号通路的激活,包括增加β-catenin水平和相关基因表达。为了证实IGF-1信号通路与Wnt/β-catenin通路在TE发育中的相互作用,我们用IGF-1受体抑制剂微足叶林培养胚胎。Picropodophyllin抑制发育参数、β-catenin水平、TE细胞分化和紧密连接形成。IGF-1和Wnt/β-catenin信号激活剂ChiR99021成功地挽救了这些效应。结论:我们的研究结果为胚胎发生过程中IGF-1与Wnt/β-catenin信号通路的相互作用提供了新的见解,并强调了IGF-1通过提高TE的形成和质量来改善生殖结果的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IGF-1 promotes trophectoderm cell proliferation of porcine embryos by activating the Wnt/β-catenin pathway.

Background: Insulin-like growth factor 1 (IGF-1) influences various aspects of embryogenesis, including embryonic development. This study investigated the effects of IGF-1 on early embryonic development in pig embryos, focusing on its interaction with the Wnt/β-catenin signaling pathway, a key regulator of cell adhesion and proliferation.

Methods: Porcine embryos were used for experiments with chemical treatments to study blastocyst development and underlying mechanism. Apoptosis, immunochemistry, gene expression, and protein quantification were performed, with statistical significance assessed.

Results: IGF-1 treatment during the early stages of embryonic development significantly enhanced developmental parameters, in particular blastocyst formation rates. Interestingly, IGF-1 increased trophectoderm (TE) cell proliferation. The TE is an essential component of the blastocyst, maintaining its structure. Successful development of pig embryos was dependent on the proper formation and function of the TE. IGF-1 upregulated the expression of functional proteins related to TE differentiation and tight junctions. Notably, these effects were more pronounced when IGF-1 treatment was performed during the last 3 days of embryonic development (days 3-6) compared to the first 3 days (days 0-3). In addition, we found that IGF-1 promoted activation of the Wnt/β-catenin signaling pathway, including increasing β-catenin levels and related gene expression. To confirm the interaction between IGF-1 signaling and the Wnt/β-catenin pathway in TE development, embryos were cultured with picropodophyllin, an IGF-1 receptor inhibitor. Picropodophyllin suppressed developmental parameters, β-catenin levels, TE cell differentiation, and tight junction formation. These effects were successfully rescued by IGF-1 and the Wnt/β-catenin signaling activator ChiR99021.

Conclusion: Our findings provide new insights into the interaction between IGF-1 and the Wnt/β-catenin signaling pathway during embryogenesis and highlight the potential of IGF-1 to improve reproductive outcomes by enhancing TE formation and quality.

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来源期刊
CiteScore
11.00
自引率
0.00%
发文量
180
期刊介绍: Cell Communication and Signaling (CCS) is a peer-reviewed, open-access scientific journal that focuses on cellular signaling pathways in both normal and pathological conditions. It publishes original research, reviews, and commentaries, welcoming studies that utilize molecular, morphological, biochemical, structural, and cell biology approaches. CCS also encourages interdisciplinary work and innovative models, including in silico, in vitro, and in vivo approaches, to facilitate investigations of cell signaling pathways, networks, and behavior. Starting from January 2019, CCS is proud to announce its affiliation with the International Cell Death Society. The journal now encourages submissions covering all aspects of cell death, including apoptotic and non-apoptotic mechanisms, cell death in model systems, autophagy, clearance of dying cells, and the immunological and pathological consequences of dying cells in the tissue microenvironment.
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