期刊
EXPERIMENTAL CELL RESEARCH
卷 412, 期 2, 页码 -出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2022.113019
关键词
Schwann cells; Sema3E; Proliferation; Migration
资金
- National Natural Science Foundation of China [31300942]
- Science and Technology Program of Nantong [JC2020034]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
Schwann cells (SCs) are crucial for peripheral nerve (PN) regeneration. This study reveals that Sema3E promotes the proliferation and migration of SCs, involving the receptors PlexinD1, Neuropilin 1 (Nrp1), and Vascular Endothelial Growth Factor Receptor 2 (VEGFR2).
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.
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