Open AccessPreserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia
Author(s) -
Chinthasagar Bastian,
Jerica Day,
Stephen Politano,
John P. Quinn,
Sylvain Brunet,
Selva Baltan
Publication year - 2019
Publication title -
neuromolecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.098
H-Index - 73
eISSN - 1559-1174
pISSN - 1535-1084
DOI - 10.1007/s12017-019-08550-w
Subject(s) - axon , mitochondrion , mitochondrial fission , white matter , microbiology and biotechnology , motility , signal transducing adaptor protein , neuroscience , axoplasmic transport , biology , ischemia , signal transduction , medicine , magnetic resonance imaging , radiology
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.