Transfer of mitochondria from astrocytes to neurons after stroke

Abstract

Recently, it was suggested that neurons can release and transfer damaged mitochondria to astrocytes for disposal and recycling 1. This ability to exchange mitochondria may represent a potential mode of cell-cell signaling in the central nervous system (CNS). Here, we show that astrocytes can also release functional mitochondria that enter into neurons. Astrocytic release of extracellular mitochondria particles was mediated by a calcium-dependent mechanism involving CD38/cyclic ADP ribose signaling. Transient focal cerebral ischemia in mice induced astrocytic mitochondria entry to adjacent neurons that amplified cell survival signals. Suppression of CD38 signaling with siRNA reduced extracellular mitochondria transfer and worsened neurological outcomes. These findings suggest a new mitochondrial mechanism of neuroglial crosstalk that may contribute to endogenous neuroprotective and neurorecovery mechanisms after stroke.

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“…Given the inordinate complexity of the mature nervous system with 10 15 connections, this topography may account for how a spatial economy of destruction is achieved in mammalian neurons when faced with the challenge of distance [45]. An equally intriguing discovery with implications for mitochondrial quality control is neuro-glial mitochondrial transfer, recently described in vitro following simulated ischemic insult [46]. Might the acquisition of healthy mitochondria serve to equilibrate network homeostasis, and how is this orchestrated with basal or induced mitophagy during ageing?…”

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“…antioxidants, anti-inflammatory agents) [15][16][17][18] into improved outcomes of critically ill patients. This issue has gradually been overcome with mandatory antioxidant vaccination programs [19] and the correction of mitochondrial damage on location by emergency medical services [20], allowing intensive care medicine to focus on supportive care rather than late "metabolic and immune damage control".…”

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