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Increased ER-mitochondria tethering promotes axon regeneration.

Soyeon Lee1,2, Wei Wang1,2, Jinyeon Hwang3

  • 1Department of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, 44919 Ulsan, South Korea.

Proceedings of the National Academy of Sciences of the United States of America
|July 24, 2019
PubMed
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Glucose regulated protein 75 (Grp75) enhances endoplasmic reticulum-mitochondria tethering at axon injury sites. This promotes axonal regeneration and functional recovery, suggesting a therapeutic strategy for nerve repair.

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ERaxon regenerationmitochondria

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Regenerative Medicine

Background:

  • Endoplasmic reticulum (ER) and mitochondria translocate to injured axons, aiding regeneration.
  • The role of ER-mitochondria tethering in injured axons remains unclear.

Purpose of the Study:

  • Investigate the existence and function of ER-mitochondria tethering in injured axons.
  • Determine if glucose regulated protein 75 (Grp75) influences ER-mitochondria tethering and axonal regeneration.

Main Methods:

  • Studied local translation of Grp75 at axon injury sites.
  • Overexpressed Grp75 in primary neurons to assess ER-mitochondria tethering and axon regrowth.
  • Analyzed mitochondrial calcium (Ca2+) levels and ATP generation.
  • Administered lentiviral vectors encoding Grp75 in an animal model of sciatic nerve crush injury.

Main Results:

  • Grp75 is locally translated at axon injury sites.
  • Grp75 overexpression enhances ER-mitochondria tethering, promoting injured axon regrowth.
  • Increased tethering boosts mitochondrial Ca2+ and ATP production, supporting axon regrowth.
  • Intrathecal Grp75 delivery improves axonal regeneration and functional recovery in sciatic nerve injury models.

Conclusions:

  • ER-mitochondria tethering, mediated by Grp75, is crucial for axonal regeneration.
  • Targeting ER-mitochondria tethering via Grp75 presents a potential therapeutic approach for nerve injury repair.