期刊
CELL REPORTS
卷 41, 期 13, 页码 -出版社
CELL PRESS
DOI: 10.1016/j.celrep.2022.111880
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类别
资金
- NIH [R01 EY19703, P30EY003790]
- Glaucoma Research Foundation
Aging leads to decline in neuronal function, but protecting astrocytes can slow down this decline and protect visual function.
Aging causes an irreversible, cumulative decline in neuronal function. Using the visual system as a model, we show that astrocytes play a critical role in maintaining retinal ganglion cell health and that deletion of SPP1 (secreted phosphoprotein 1, or osteopontin) from astrocytes leads to increased vulnerability of ganglion cells to age, elevated intraocular pressure, and traumatic optic nerve damage. Overexpression of SPP1 slows the age-related decline in ganglion cell numbers and is highly protective of visual function in a mouse model of glaucoma. SPP1 acts by promoting phagocytosis and secretion of neurotrophic factors while inhibiting pro-duction of neurotoxic and pro-inflammatory factors. SPP1 up-regulates transcription of genes related to oxidative phosphorylation, functionally enhances mitochondrial respiration, and promotes the integrity of mitochondrial microstructure. SPP1 increases intracellular ATP concentration via up-regulation of VDAC1.
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