Abstract
BackgroundSchwann 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.ResultsSPP1 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.ConclusionThese 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.
Highlights
Schwann cells (SCs) play a crucial role in Wallerian degeneration after peripheral nerve injury
These results suggested that Secreted phosphoprotein 1 (SPP1) promoted proliferation and inhibited apoptosis of SCs through Protein kinase C alpha (PKCα) signaling pathway by binding with CD44 and αvβ3
SPP1 and PKCα were increased in SCs after peripheral nerve injury in human specimens In our previous study, we found the expression of SPP1 and PKCα was upregulated after rat sciatic nerve injury [23, 24]
Summary
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. How do these genes regulate the proliferation and apop‐ tosis of SCs remains unclear. SCs and support the survival of injured neurons, which makes them potential targets for therapeutic interventions [11,12,13] How do these genes control the proliferation and survival of SCs remains unclear, making it difficult to manipulate SCs for therapeutic purposes. Our previous study suggested that the expression of SPP1 was up-regulated after sciatic nerve injury in rats, and elevated SPP1 promoted the proliferation and inhibited the apoptosis of SCs [23]. Our early study found that PKCα promoted the proliferation of SCs by activating ERK signaling pathways [24], which led to the hypothesis that SPP1 promoted cell proliferation and inhibited apoptosis of SCs through PKCα signaling pathways
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