Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia

Chinthasagar Bastian, Jerica Day, Stephen Politano, John Quinn, Sylvain Brunet, Selva Baltan

Research output: Contribution to journalArticlepeer-review

Abstract

Stroke significantly affects white matter in the brain by impairing axon function, which results in clinical deficits. Axonal mitochondria are highly dynamic and are transported via microtubules in the anterograde or retrograde direction, depending upon axonal energy demands. Recently, we reported that mitochondrial division inhibitor 1 (Mdivi-1) promotes axon function recovery by preventing mitochondrial fission only when applied during ischemia. Application of Mdivi-1 after injury failed to protect axon function. Interestingly, L-NIO, which is a NOS3 inhibitor, confers post-ischemic protection to axon function by attenuating mitochondrial fission and preserving mitochondrial motility via conserving levels of the microtubular adaptor protein Miro-2. We propose that preventing mitochondrial fission protects axon function during injury, but that restoration of mitochondrial motility is more important to promote axon function recovery after injury. Thus, Miro-2 may be a therapeutic molecular target for recovery following a stroke.

Original languageEnglish (US)
Pages (from-to)484-492
Number of pages9
JournalNeuroMolecular Medicine
Volume21
Issue number4
DOIs
StatePublished - Dec 1 2019
Externally publishedYes

Keywords

  • Ischemia
  • Miro-2
  • Mitochondria
  • Mitochondrial dynamics
  • NOS3
  • Stroke

ASJC Scopus subject areas

  • Molecular Medicine
  • Neurology
  • Cellular and Molecular Neuroscience

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