Young Astrocytic Mitochondria Attenuate the Elevated Level of CCL11 in the Aged Mice, Contributing to Cognitive Function Improvement
Open accessAbstract
Aging drives cognitive decline, and mitochondrial dysfunction is a hallmark of age-induced neurodegeneration. Recently, we demonstrated that astrocytes secrete functional mitochondria (Mt), which help adjacent cells to resist damage and promote repair after neurological injuries. However, the relationship between age-dependent changes in astrocytic Mt function and cognitive decline remains poorly understood. Here, we established that aged astrocytes secret less functional Mt compared to young astrocytes. We found the aging factor C-C motif chemokine 11 (CCL11) is elevated in the hippocampus of aged mice, and that its level is reduced upon systemic administration of young Mt, in vivo. Aged mice receiving young Mt, but not aged Mt improved cognitive function and hippocampal integrity. Using a CCL11-induced aging-like model in vitro, we found that astrocytic Mt protect hippocampal neurons and enhance a regenerative environment through upregulating synaptogenesis-related gene expression and anti-oxidants that were suppressed by CCL11. Moreover, the inhibition of CCL11-specific receptor C-C chemokine receptor 3 (CCR3) boosted the expression of synaptogenesis-related genes in the cultured hippocampal neurons and restored the neurite outgrowth. This study suggests that young astrocytic Mt can preserve cognitive function in the CCL11-mediated aging brain by promoting neuronal survival and neuroplasticity in the hippocampus.
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CCL11/Eotaxin1 is a chemokine that selectively recruits eosinophils, is elevated with age in humans and mice, and promotes senescence.
“CCL11/Eotaxin1 is a chemokine that selectively recruits eosinophils, is elevated with age in humans and mice52–54, and has been shown to promote senescence55.”
From Senescent-like microglia limit remyelination through the senescence associated secretory phenotype (2025) · cites this paper as [53]
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Mitochondria and brain aging: From cell-specific dysfunction to intercellular cooperation
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- Authors
- Tashiro, R., Ozaki, D., Bautista-Garrido, J., Sun, G., Obertas, L., Mobley, A. S., Kim, G. S., Aronowski, J., & Jung, J. E.
- Affiliations
- The University of Texas Health Science Center at Houston (US)
- Corresponding author
- Jung, Joo Eun
- ORCID
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2023-03-08
- Volume
- 24
- Issue
- 6
- Pages
- 5187
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC10049211
- OpenAlex
- W4323665354
- Cited by
- 15
- References
- 89
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 1 · 2023: 2
- FWCI
- 1.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Commons-TMC (Texas Medical Center) (submittedVersion)
- Funders
- UTHealth
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- mitochondrial transfer, eotaxin, CCR3, aging, cognitive decline, hippocampus, synaptogenesis, neuroplasticity, neuronal survival, mitochondrial dysfunction, aged mice, neurite outgrowth
- MeSH terms
- Animals, Astrocytes, Brain, Cognition, Hippocampus, Mitochondria, Neurons, Mice, Chemokine CCL11
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