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<p>Collagen type XX alpha 1 (COL20A1) was recently found to be highly concentrated in perisynaptic Schwann cells (PSCs), the synaptic glia of the neuromuscular junction (NMJ), suggesting that COL20A1 plays important roles in PSCs and at the NMJ. To investigate this possibility, we generated mice lacking Col20a1 only in Schwann cells (Col20a1-SCKO) and globally (Col20a1-gKO). PSCs and NMJs were morphologically unchanged in adult Col20a1-SCKO mice despite these conditional mice exhibiting gait abnormalities. Additional analysis revealed roles of COL20A1 at regenerating NMJs. We found that loss of COL20A1 altered the time course of migrating Schwann cells associated with NMJs. It also inhibited the remodeling of the post-synaptic region that naturally occurs following reinnervation. However, the timing of NMJ reinnervation was unchanged in Col20a1-SCKO compared to control mice. We next examined adult Col20a1-gKO mice. These mice did not exhibit overt morphological differences compared to control mice. Col20a1-gKO mice also did not exhibit NMJ alterations despite presenting with increased mass of the extensor digitorum longus and soleus muscles. Together, these data provide important leads about potential roles of COL20A1 in healthy and injured adult PSCs, NMJs, and muscles.</p>

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Loss of COL20A1 in Schwann Cells Alters Regeneration of the Neuromuscular Junction and Locomotor Activity in Mice

  • 期刊论文

  • 发表日期：

    2025年9月4日

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  • Robert Louis Hastings,
  • William Boyce,
  • Devin Juros,
  • Jinho Kim,
  • Zaid Khan,
  • Aatish Sethi,
  • Gregorio Valdez

摘要

Collagen type XX alpha 1 (COL20A1) was recently found to be highly concentrated in perisynaptic Schwann cells (PSCs), the synaptic glia of the neuromuscular junction (NMJ), suggesting that COL20A1 plays important roles in PSCs and at the NMJ. To investigate this possibility, we generated mice lacking Col20a1 only in Schwann cells (Col20a1-SCKO) and globally (Col20a1-gKO). PSCs and NMJs were morphologically unchanged in adult Col20a1-SCKO mice despite these conditional mice exhibiting gait abnormalities. Additional analysis revealed roles of COL20A1 at regenerating NMJs. We found that loss of COL20A1 altered the time course of migrating Schwann cells associated with NMJs. It also inhibited the remodeling of the post-synaptic region that naturally occurs following reinnervation. However, the timing of NMJ reinnervation was unchanged in Col20a1-SCKO compared to control mice. We next examined adult Col20a1-gKO mice. These mice did not exhibit overt morphological differences compared to control mice. Col20a1-gKO mice also did not exhibit NMJ alterations despite presenting with increased mass of the extensor digitorum longus and soleus muscles. Together, these data provide important leads about potential roles of COL20A1 in healthy and injured adult PSCs, NMJs, and muscles.