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<p>Adult neural stem cells (NSCs) offer a promising avenue for restoring spinal cord injury (SCI). However, their precise identity in the mammalian spinal cord remains unclear. Our previous research demonstrated that Pkd2l1-positive cerebrospinal fluid-contacting neurons (CSF-cNs) possess the NSC properties. Furthermore, understanding the role and molecular mechanisms of CSF-cNs as endogenous NSCs in spinal cord repair is crucial for developing effective treatments. This study utilizes a Pkd2l1<sup>−/−</sup> transgenic mouse model to investigate the role of CSF-cNs in SCI repair. We found that the CSF-cN population was almost absent in Pkd2l1<sup>−/−</sup> mice. Following SCI, these mice exhibited a significant reduction in the number of NSCs surrounding the central canal. Notably, Pkd2l1<sup>−/−</sup> mice showed impaired neuronal regeneration and compromised motor function recovery post-SCI. These findings highlight the potential importance of Pkd2l1 as a target for treating SCI by focusing on endogenous NSCs.</p>

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Pkd2l1 deletion inhibits the neurogenesis of cerebrospinal fluid-contacting neurons and impedes spinal cord injury repair

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月23日

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  • Yi Zhang,
  • Liang Cao,
  • Haijian Yan,
  • Zhangrong Luo,
  • Chanjuan Chen,
  • Zeyu Shangguan,
  • Qizhe Li,
  • Xuexing Shi,
  • Leiluo Yang,
  • Wei Tan,
  • Shengxin Yang,
  • Jiangquan Fu,
  • Chunqing Wang,
  • Xiaowei Dou,
  • Qing Li

摘要

Adult neural stem cells (NSCs) offer a promising avenue for restoring spinal cord injury (SCI). However, their precise identity in the mammalian spinal cord remains unclear. Our previous research demonstrated that Pkd2l1-positive cerebrospinal fluid-contacting neurons (CSF-cNs) possess the NSC properties. Furthermore, understanding the role and molecular mechanisms of CSF-cNs as endogenous NSCs in spinal cord repair is crucial for developing effective treatments. This study utilizes a Pkd2l1−/− transgenic mouse model to investigate the role of CSF-cNs in SCI repair. We found that the CSF-cN population was almost absent in Pkd2l1−/− mice. Following SCI, these mice exhibited a significant reduction in the number of NSCs surrounding the central canal. Notably, Pkd2l1−/− mice showed impaired neuronal regeneration and compromised motor function recovery post-SCI. These findings highlight the potential importance of Pkd2l1 as a target for treating SCI by focusing on endogenous NSCs.