Overview: Astrocytes improve healing after a brain hemorrhage by transferring their mitochondria to damaged neurons.
After a brain hemorrhage, neural support cells called astrocytes enhance healing by transferring their mitochondria to damaged neurons.
The 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 flows into the tissue, causing free radicals that do even more damage.
The hemorrhage damages mitochondria, the site of energy production in cells. After a hemorrhage, astrocytes transfer their mitochondria to damaged neurons.
These healthy mitochondria contain a “healing” peptide called humanin and an enzyme called manganese superoxide dismutase (Mn-SOD) that help neutralize free radicals.
Tasiro et al. mice injected with healthy mitochondria after hemorrhage. The hemorrhage decreased the levels of Mn-SOD in the mouse brain and increased the number of free radicals.
Using molecular tags, the researchers found that the rodents’ neurons picked up the mitochondria from the bloodstream.
The mice that received the treatment showed improved neurological recovery, but the benefits diminished when the mice were given mitochondria without the Mn-SOD enzyme.
These results show that mitochondria can be transferred between brain cells to improve health and promote recovery.
About this neuroscience research news
Author: Calli McMurray
Contact: Calli McMurray – SfN
Image: The image is attributed 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
Transplantation of astrocytic mitochondria modulates neuronal antioxidant defense and neuroplasticity and promotes functional recovery after intracerebral hemorrhage
Astrocytes release functional mitochondria (Mt) that play regulatory and pro-survival functions when entering adjacent cells. We recently demonstrated that these released Mt can invade microglia to promote their restorative/pro-phagocytic phenotype that aids in hematomas clearance and neurological recovery after intracerebral hemorrhage (ICH).
However, a relevance of astrocytic Mt transfer to neurons in protecting the brain after ICH is unclear. Here we found that ICH causes a robust increase in superoxide formation and increased oxidative damage that coincides 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 entry into the brain (and neurons), restored Mn-SOD levels and reduced neurological deficits in male mice subjected to ICH. using one in vitro ICH-like injury model in cultured neurons, we determined that astrocytic Mt upon entry into neurons prevented reactive oxygen species-induced oxidative stress and neuronal death by restoring neuronal Mn-SOD levels, while simultaneously inhibiting neurite expansion and upregulation of synaptogenesis-related gene expression. .
Furthermore, we found that Mt genome-encoded small peptide humanin (HN) normally abundant in Mt could simulate the Mt transfer effect on neuronal Mn-SOD expression, oxidative stress and neuroplasticity under ICH-like damage.
This study demonstrates that adoptive astrocytic Mt transfer enhances neuronal Mn-SOD-mediated anti-oxidative defense and neuroplasticity in the brain, enhancing functional recovery after ICH.