Platelets are critical regulators of liver regeneration, but the mechanisms are still not fully understood. Platelets have been shown to contain a wide variety of microRNAs (miRNAs) and play an important role in many diseases. However, the mechanism that how the platelet microparticles (PMPs)‐derived miRNA regulate the hepatocyte proliferation is not very clear. In this study, we have successfully isolated and identified PMPs. We also found that PMPs, which could be well integrated into the HHL‐5 cells, could upregulate the level of miR‐25‐3p in HHL‐5 cells. Meanwhile, we found that PMPs‐derived miR‐25‐3p promoted HHL‐5 cells proliferation by accelerating cells into the S phase, and enhanced the autophagy by increasing the LC3II expression and reducing the P62 expression. Then, we proved that the miR‐25‐3p could target the B‐cell translocation gene 2 (BTG2) and downregulate the expression levels of the BTG2 gene in HHL‐5 cells. In addition, the overexpression of BTG2 significantly inhibited the proliferation and autophagy abilities of HHL‐5 cells, while cotransfected miR‐25‐3p mimics or PMPs could partially rescue HHL‐5 cells proliferation and autophagy. Furthermore, we proved that PMPs accelerated hepatocyte proliferation by regulating autophagy pathways. Therefore, PMPs‐derived miR‐25‐3p promoted HHL‐5 cell proliferation and autophagy by targeting BTG2, which may be a new therapeutic method for liver regeneration.

中文翻译：

---

血小板微粒衍生的 miR-25-3p 通过减少 B 细胞易位基因 2 促进肝细胞增殖和细胞自噬。

血小板是肝再生的关键调节因子，但其机制仍不完全清楚。血小板已被证明含有多种 microRNA (miRNA)，并在许多疾病中发挥重要作用。然而，血小板微粒（PMPs）来源的miRNA如何调节肝细胞增殖的机制尚不清楚。在这项研究中，我们成功地分离和鉴定了PMP。我们还发现，PMPs 可以很好地整合到 HHL-5 细胞中，可以上调 HHL-5 细胞中 miR-25-3p 的水平。同时，我们发现PMPs衍生的miR-25-3p通过加速细胞进入S期来促进HHL-5细胞增殖，并通过增加LC3II表达和减少P62表达来增强自噬。然后，我们证明miR-25-3p可以靶向B细胞易位基因2（BTG2）并下调HHL-5细胞中BTG2基因的表达水平。此外，BTG2的过表达显着抑制HHL-5细胞的增殖和自噬能力，而共转染miR-25-3p模拟物或PMP可以部分挽救HHL-5细胞的增殖和自噬能力。此外，我们证明PMPs通过调节自噬途径加速肝细胞增殖。因此，PMPs衍生的miR-25-3p通过靶向BTG2促进HHL-5细胞增殖和自噬，这可能是肝再生的新治疗方法。