Source: SfN
After a brain hemorrhage, neural support cells called astrocytes enhance healing by transferring their mitochondria to damaged neurons.
Healthy mitochondria stimulate the production of an enzyme that fights free radicals, according to new research published in Journal of Neuroscience.
An artery in the brain bursts. Blood enters the tissue, inducing free radicals that cause even more damage.
Bleeding damages mitochondria, the site of energy production in cells. Astrocytes transfer their mitochondria to damaged neurons after hemorrhage.
These healthy mitochondria contain a “healing” peptide called humanin and an enzyme called manganese superoxide dismutase (Mn-SOD) that help neutralize free radicals.
Tashiro et al. mice injected with healthy mitochondria after hemorrhage. Hemorrhage reduced the levels of Mn-SOD in the brains of mice and increased the number of free radicals.
Using molecular tags, the researchers found that rodent neurons took up mitochondria from the bloodstream.
Mice that received the treatment showed improved neurological recovery, but the benefits were diminished if the mice were given mitochondria without the Mn-SOD enzyme.
These results reveal that mitochondria can be transferred between brain cells to improve health and aid recovery.
About this neuroscience research news
Author: Callie McMurray
Source: SfN
Contact: Calli McMurray – SfN
Image: Image is credited to Tashiro et al., JNeurosci 2022
Original Research: Closed access
“Transplantation of astrocytic mitochondria modulates neuronal antioxidant defense and neuroplasticity and promotes functional recovery after intracerebral hemorrhage” by Tashiro et al. Journal of Neuroscience
Summary
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Transplantation of astrocytic mitochondria modulates neuronal antioxidant defense and neuroplasticity and promotes functional recovery after intracerebral hemorrhage
Astrocytes release functional mitochondria (Mt) that have pro-survival and regulatory functions upon entry into adjacent cells. We recently demonstrated that these released Mt could enter microglia to promote their reparative/prophagocytic phenotype that aids in hematoma clearance and neurological recovery after intracerebral hemorrhage (ICH).
However, the relevance of astrocytic Mt transfer to neurons in protecting the brain after ICH is unclear. Here, we found that ICH results in a robust increase in superoxide generation and elevated oxidative damage coinciding with the loss of the mitochondrial enzyme manganese superoxide dismutase (Mn-SOD).
The deleterious effect of ICH was reversed by intravenous transplantation of astrocytic Mt which, upon entering the brain (and neurons), restored Mn-SOD levels and reduced neurological deficits in male mice subjected to ICH . Using a in vitro model of ICH-like injury in cultured neurons, we established that astrocytic Mt upon entering neurons prevented reactive oxygen species-induced oxidative stress and neuronal death by restoring neuronal Mn-SOD levels , while promoting neurite extension and up-regulation of synaptogenesis. gene expression
Furthermore, we found that the small peptide humanin (HN) encoded by the Mt genome that is normally abundant in Mt, could mimic the transfer effect of Mt on the neuronal expression of Mn-SOD, oxidative stress and neuroplasticity under ICH-like lesions.
This study demonstrates that adoptive astrocytic Mt transfer enhances Mn-SOD-mediated antioxidant defense and neuronal neuroplasticity in the brain, which potentiate functional recovery after ICH.