Platelet-rich plasma (PRP) and its byproduct platelet-poor plasma (PPP) are rich sources of cytokines in tissue damage repair. Bone marrow-derived mesenchymal stem cells (BM-MSCs) have received more and more attention for their ability to treat multiple diseases. The purpose of our study was to investigate the biologic action of PPP and PRP on BM-MSCs. The adipogenic potential of BM-MSCs revealed no obvious change, but the osteogenic ability of BM-MSCs was enhanced after treated with PRP. CCK8 assays and cell colony formation assays showed that PRP promoted cell proliferation, while this effect of PPP was not obvious. No obvious difference was found in cell cycle and apoptosis of BM-MSCs between PRP and PPP treatment. Expression of β-galactosidase, a biological marker of senescence, was decreased upon PRP treatment which indicated that PRP provided significant protection against cellular senescence. The migratory capacity of BM-MSCs was detected by scratch and transwell assays. The results indicated that PRP could affect the migration ability of BM-MSCs. From immunofluorescence detection and western blot, we demonstrated that the level of epithelial-mesenchymal transition-related proteins was changed and several pluripotency marker genes, including Sox2, Sall4, Oct4, and Nanog, were increased. Finally, the expression of the key signal pathway such as PI3K/AKT was examined. Our findings suggested that PRP promoted cell migration of BM-MSCs via stimulating the signaling pathway of PI3K/AKT.

中文翻译：

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富血小板血浆和贫血小板血浆对 BM-MSCs 体外生物学特性的影响。

富血小板血浆 (PRP) 及其副产物贫血小板血浆 (PPP) 是组织损伤修复中细胞因子的丰富来源。骨髓间充质干细胞（BM-MSCs）因其治疗多种疾病的能力而受到越来越多的关注。我们研究的目的是研究 PPP 和 PRP 对 BM-MSC 的生物学作用。BM-MSCs的成脂潜能未见明显变化，但经PRP处理后BM-MSCs的成骨能力增强。CCK8测定和细胞集落形成测定显示PRP促进细胞增殖，而PPP的这种作用不明显。PRP和PPP处理之间BM-MSCs的细胞周期和凋亡未发现明显差异。β 的表达β-半乳糖苷酶是衰老的生物标志物，在 PRP 处理后降低，这表明 PRP 提供了显着的细胞衰老保护。BM-MSCs 的迁移能力通过划痕和 transwell 试验检测。结果表明PRP可以影响BM-MSCs的迁移能力。通过免疫荧光检测和蛋白质印迹，我们证明上皮-间充质转化相关蛋白的水平发生了变化，并且包括 Sox2、Sall4、Oct4 和 Nanog 在内的几种多能性标记基因增加。最后，检测了关键信号通路如 PI3K/AKT 的表达。我们的研究结果表明，PRP 通过刺激 PI3K/AKT 的信号通路促进 BM-MSCs 的细胞迁移。