Neurons Release Injured Mitochondria as "Help-Me" Signaling After Ischemic Stroke.

ABSTRACT: Mitochondrial dysfunction has been regarded as one of the major contributors of ischemic neuronal death after stroke. Recently, intercellular mitochondrial transfer between different cell types has been widely studied and suggested as a potential therapeutic approach. However, whether mitochondria are involved in the neuron-glia cross-talk following ischemic stroke and the underlying mechanisms have not been explored yet. In this study, we demonstrated that under physiological condition, neurons release few mitochondria into the extracellular space, and the mitochondrial release increased when subjected to the challenges of acidosis, hydrogen peroxide (H₂O₂), N-methyl-D-aspartate (NMDA), or glutamate. Acidosis reduced the mitochondrial basal respiration and low

SUBMITTER: Gao L 

PROVIDER: S-EPMC8926840 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature