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首页> 外文期刊>Journal of cellular physiology. >PTHrP promotes development of mouse preimplantation embryos through the AKT/cyclin D1 pathway and nuclear translocation of HDAC4
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PTHrP promotes development of mouse preimplantation embryos through the AKT/cyclin D1 pathway and nuclear translocation of HDAC4

机译：鼠标PTHrP促进发展胚胎植入前的胚胎通过一种蛋白激酶/细胞周期蛋白D1HDAC4通路和核易位

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摘要

Parathyroid hormone-related protein (PTHrP), the main cause of humoral hy-percalcemia in malignancies, promotes cell proliferation and delays terminal cell maturation during embryonic development. Our previous study reported that PTHrP plays important roles in blastocyst formation, pluripotency gene expression, and histone acetylation during mouse preimplantation embryonic development. In this study, we further investigated the mechanism of preimplantation embryonic development regulated by PTHrP. Our results showed that Pthrp depletion decreased both the developmental rate of embryos at the cleavage stage and the cell number of morula-stage embryos. Pthrp-depleted embryos had significantly decreased levels of cyclin D1, phospho (p)-AKT (Thr308) and E2F1. However, Pthrp depletion did not cause significant changes in CDK4, β-catenin or RUNX2 expression. In addition, our results indicated that Pthrp depletion promoted HDAC4 translocation from the cytoplasm to the nucleus in cleavage-stage embryos by stimulating the activity of protein phosphatase 2A (PP2A), which resulted in depho-sphorylation of HDAC4. Taken together, these results suggest that PTHrP regulates cleavage division progression and blastocyst formation through the AKT/cyclin D1 pathway and that PTHrP modulates histone acetylation patterns through nuclear translocation of HDAC4 via PP2A-dependent HDAC4 dephosphorylation during preimplantation embryonic development in mice.
机译：甲状旁腺与荷尔蒙相关的蛋白质(PTHrP)体液hy-percalcemia的主要原因促进细胞增殖和恶性肿瘤延迟终端在胚胎细胞成熟发展。PTHrP在胚泡中扮演重要角色形成、多能性基因表达和在老鼠胚胎植入前的组蛋白乙酰化作用胚胎发育。胚胎植入前的调查机制胚胎发育由PTHrP规定。结果表明,Pthrp损耗减少胚胎的发育率卵裂阶段和细胞的数量morula-stage胚胎。细胞周期蛋白D1的水平显著下降磷(p)一种蛋白激酶(Thr308)和E2F1。损耗没有造成重大的变化到,β连环蛋白或RUNX2表达式。我们的研究结果表明,Pthrp损耗从细胞质中提升HDAC4易位在卵裂时期胚胎细胞核刺激蛋白磷酸酶的活性2 (PP2A),这导致depho-sphorylationHDAC4。PTHrP调节乳沟分裂进展和胚泡形成一种蛋白激酶/细胞周期蛋白D1通路,PTHrP调节组蛋白乙酰化作用通过核模式易位的HDAC4通过PP2A-dependent HDAC4在胚胎植入前的脱磷酸化胚胎发育中老鼠。

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