雪旺细胞(SCs)在周围神经(PN)再生中发挥重要作用,migrate,为PN损伤后轴突再生提供营养支持。然而,潜在的机制仍然部分理解。Semaphorin3E(Sema3E),Sema3s家族的一员,是一种分泌的分子,在轴突导向和发育和缺血后血管生成的抑制剂中被称为排斥线索。在这项研究中,我们检测了Sema3E在坐骨神经和SCs中的表达,并探讨了Sema3E对SCs增殖和迁移的影响。免疫荧光和ELISA分析显示,Sema3E在坐骨神经SCs中的表达和培养的SCs分泌Sema3E,分别。外源性Sema3E促进SC增殖和迁移,而通过siRNA转染抑制内源性Sema3E减弱SC的增殖和迁移。此外,阻断受体Neuropilin1(Nrp1),PlexinD1和血管内皮生长因子受体2(VEGFR2)通过中和抗体或抑制剂抑制Sema3E对SC的促进作用。这项研究表明,Sema3E促进SC的增殖和迁移,以及受体PlexinD1,Nrp1和VEGFR2参与这些过程。这项研究扩展了我们对神经损伤过程中调节SC表型的机制的理解,并为促进PN再生提供了潜在的靶标。
Schwann cells (SCs) play a critical role in peripheral nerve (PN) regeneration because of their ability to proliferate, migrate, and provide trophic support for axon regeneration after PN injury. However, the underlying mechanism is still partially understood. Semaphorin3E (
Sema3E), a member of the Sema3s family, is a secreted molecular known as a repelling cue in axon guidance and inhibitor of developmental and postischemic angiogenesis. In this study, we examined the expression of
Sema3E in sciatic nerves and SCs and explored the effects of
Sema3E on SCs proliferation and migration. Immunofluorescence and ELISA analyses illustrated the expression of Sema3E in SCs of Sciatic nerves and the secretion of
Sema3E by cultured SCs, respectively. Exogenous
Sema3E promoted SC proliferation and migration while knockdown of the endogenous
Sema3E by siRNA transfection attenuated proliferation and migration of SCs. Furthermore, blocking the receptor Neuropilin 1 (Nrp1), PlexinD1 and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) by neutralizing antibody or inhibitor suppressed the promoting effects of Sema3E on SCs. This study indicated that Sema3E promoted SC proliferation and migration and the involvement of receptor PlexinD1, Nrp1, and VEGFR2 in these processes. This study extended our understanding of the mechanism that modulated SC phenotype during nerve injury and provided a potential target for promoting PN regeneration.