Motoneuron-Specific PTEN Deletion in Mice Induces Neuronal Hypertrophy and Regeneration After Facial Nerve Injury

    Christopher Meyer zu Reckendorf, Diana Moser, Anna Blechschmidt, Venkata Neeha Joga, Daniela Sinske, Jutta Hegler, Sören‐Oliver Deininger, Alberto Catanese, Sabine Vettorazzi, Gregor Antoniadis, Tobias M. Boeckers, Bernd Knöll
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    TLDR Deleting the PTEN gene in mice causes nerve cells to grow larger and heal better after injury, but may cause overgrowth and hair loss in older mice.
    This study investigated the role of the tumor suppressor gene PTEN in neuronal morphology and axon regeneration in mice. Researchers conditionally deleted PTEN from mouse facial motoneurons and observed the effects both with and without peripheral facial nerve injury. They found that PTEN deletion led to neuronal hypertrophy and improved regeneration and recovery of whisker movement after nerve injury, through upregulation of a signaling pathway involving P-CREB, P-Akt, P-PRAS40, P-mTOR, and P-4EBP1. However, in aged mice (12 months), PTEN deletion resulted in hair loss and facial hyperplasia, indicating potential negative effects in older animals. The study concludes that while PTEN loss can stimulate axon growth after injury in younger mice, it may also lead to hyperplasia in older mice, demonstrating the complex role of TSGs in neuron function and regeneration.
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