Schwann cells (SCs) play a crucial role in Wallerian degeneration after peripheral nerve injury. The expression of genes in SCs undergo a series of changes, which greatly affect the proliferation and apoptosis of SCs as well as the fate of peripheral nerve regeneration. However, how do these genes regulate the proliferation and apoptosis of SCs remains unclear. SPP1 and PKCα were found upregulated after human median peripheral nerve injury, which promoted SCs proliferation and survival. The promoted proliferation and inhibited apoptosis by SPP1 were blocked after the treatment of PKCα antagonist Gö6976. Whereas, the inhibited proliferation and enhanced apoptosis induced by silence of SPP1 could be rescued by the activation of PKCα, which suggested that SPP1 functioned through PKCα. Moreover, both CD44 and αvβ3 were found expressed in SCs and increased after peripheral nerve injury. Silence of CD44 or β3 alleviated the increased proliferation and inhibited apoptosis induced by recombinant osteopontin, suggesting the function of SPP1 on SCs were dependent on CD44 and β3. These results suggested that SPP1 promoted proliferation and inhibited apoptosis of SCs through PKCα signaling pathway by binding with CD44 and αvβ3. This study provides a potential therapeutic target for improving peripheral nerve recovery.

中文翻译：

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SPP1 在周围神经损伤后通过与 CD44 和 αvβ3 结合，通过 PKCα 促进雪旺氏细胞增殖和存活。

雪旺细胞 (SCs) 在周围神经损伤后的沃勒变性中起关键作用。SCs中基因的表达发生了一系列变化，极大地影响了SCs的增殖和凋亡以及周围神经再生的命运。然而，这些基因如何调节 SCs 的增殖和凋亡仍不清楚。在人正中外周神经损伤后发现 SPP1 和 PKCα 上调，促进 SCs 增殖和存活。在 PKCα 拮抗剂 Gö6976 处理后，SPP1 促进的增殖和抑制的细胞凋亡被阻断。而由SPP1沉默诱导的增殖抑制和细胞凋亡增强可以通过PKCα的激活来挽救，这表明SPP1通过PKCα发挥作用。而且，发现 CD44 和 αvβ3 在 SCs 中表达并在周围神经损伤后增加。CD44或β3的沉默减轻了重组骨桥蛋白诱导的增殖增加并抑制了细胞凋亡，表明SPP1对SCs的功能依赖于CD44和β3。这些结果表明，SPP1通过与CD44和αvβ3结合，通过PKCα信号通路促进SCs增殖并抑制细胞凋亡。该研究为改善周围神经恢复提供了潜在的治疗靶点。这些结果表明，SPP1通过与CD44和αvβ3结合，通过PKCα信号通路促进SCs增殖并抑制细胞凋亡。该研究为改善周围神经恢复提供了潜在的治疗靶点。这些结果表明，SPP1通过与CD44和αvβ3结合，通过PKCα信号通路促进SCs增殖并抑制细胞凋亡。该研究为改善周围神经恢复提供了潜在的治疗靶点。