In the developing peripheral nervous system, Schwann cells (SCs) extend their processes to contact, sort, and myelinate axons. The mechanisms that contribute to the interaction between SCs and axons are just beginning to be elucidated. Using a SC‐neuron coculture system, we demonstrate that Arg‐Gly‐Asp (RGD) peptides that inhibit α_V‐containing integrins delay the extension of SCs elongating on axons. α_V integrins in SC localize to sites of contact with axons and are expressed early in development during radial sorting and myelination. Short interfering RNA‐mediated knockdown of the α_V integrin subunit also delays SC extension along axons in vitro, suggesting that α_V‐containing integrins participate in axo‐glial interactions. However, mice lacking the α_V subunit in SCs, alone or in combination with the potentially compensating α₅ subunit, or the α_V partners β₃ or β₈, myelinate normally during development and remyelinate normally after nerve crush, indicating that overlapping or compensatory mechanisms may hide the in vivo role of RGD‐binding integrins.

中文翻译：

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雪旺细胞中的 αV 整合素促进与轴突的附着，但在体内是可有可无的。

在发育中的周围神经系统中，雪旺细胞 (SC) 将其过程扩展到接触、分类和髓鞘化轴突。促成 SCs 和轴突之间相互作用的机制才刚刚开始被阐明。使用 SC-神经元共培养系统，我们证明了抑制含有 αV 的整合素的 Arg-Gly-Asp (RGD) 肽_延迟了 SCs 在轴突上的延伸。SC 中的α _V整合素定位于与轴突接触的部位，并在径向分选和髓鞘形成过程中的早期发育过程中表达。短干扰 RNA 介导的 α _V整合素亚基敲低也延迟了体外 SC 沿轴突的延伸，这表明 α _V含整合素参与轴突-胶质细胞相互作用。然而，在 SCs 中缺乏 α _V亚基的小鼠，单独或与潜在的补偿性 α ₅亚基或 α _V伙伴 β ₃或 β ₈组合，在发育过程中正常髓鞘形成，在神经挤压后正常髓鞘再生，表明重叠或补偿机制可能隐藏 RGD 结合整合素的体内作用。