Reactive Astrocytes Promote ALS-like Degeneration and Intracellular Protein Aggregation in Human Motor Neurons by Disrupting Autophagy through TGF-β1
Open accessAbstract
Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing motor neuron disease. Astrocytic factors are known to contribute to motor neuron degeneration and death in ALS. However, the role of astrocyte in promoting motor neuron protein aggregation, a disease hallmark of ALS, remains largely unclear. Here, using culture models of human motor neurons and primary astrocytes of different genotypes (wild-type or SOD1 mutant) and reactive states (non-reactive or reactive), we show that reactive astrocytes, regardless of their genotypes, reduce motor neuron health and lead to moderate neuronal loss. After prolonged co-cultures of up to 2 months, motor neurons show increased axonal and cytoplasmic protein inclusions characteristic of ALS. Reactive astrocytes induce protein aggregation in part by releasing transforming growth factor β1 (TGF-β1), which disrupts motor neuron autophagy through the mTOR pathway. These results reveal the important contribution of reactive astrocytes in promoting aspects of ALS pathology independent of genetic influences.
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Reactive astrocytes from SOD1 transgenic mice secrete TGFB1, which stimulates MTOR signaling and impairs autophagy in co-cultured motor neurons.
“reactive astrocytes from SOD1 transgenic mice secrete TGFB1, which stimulates MTOR signaling and impairs autophagy in co-cultured motor neurons [415]”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [415]
Astrocytes are both necessary and sufficient for neurodegeneration in this ALS model.
“implying that astrocytes are both necessary and sufficient for neurodegeneration in this ALS model.”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [415]
Conditioned media from SOD1-expressing astrocytes is toxic to cultured human motor neurons in vitro.
“conditioned media from SOD1-expressing astrocytes is toxic to cultured human motor neurons in vitro [181,415]”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [415]
Astrocytes can exacerbate neuronal toxicity by compromising neuronal proteostasis in a non-cell autonomous fashion.
“suggesting that astrocytes can exacerbate neuronal toxicity by compromising neuronal proteostasis in a non-cell autonomous fashion.”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [415]
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- Authors
- Tripathi, P., Rodriguez-Muela, N., Klim, J. R., de Boer, A. S., Agrawal, S., Sandoe, J., Lopes, C. S., Ogliari, K. S., Williams, L. A., Shear, M., Rubin, L. L., Eggan, K., & Zhou, Q.
- Affiliations
- Harvard University (US)
- Corresponding author
- Zhou, Qiao
- Venue
- Stem Cell Reports
- Publisher
- Elsevier BV
- Published
- 2017-08
- Volume
- 9
- Issue
- 2
- Pages
- 667-680
- ISSN
- 2213-6711 (ISSN-L)
- PMC
- PMC5549875
- OpenAlex
- W2735021289
- Cited by
- 123
- References
- 64
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 18 · 2023: 12 · 2022: 17 · 2021: 19 · 2020: 14 · 2019: 15 · 2018: 14 · 2017: 1
- FWCI
- 8.38
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Stem Cell Reports (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Harvard Stem Cell Institute (DP-0065-10-00)
- Topics
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyotrophic lateral sclerosis, reactive astrocytes, motor neuron degeneration, protein aggregation, TGF-β1, autophagy, mTOR signaling, cytoplasmic inclusions
- MeSH terms
- Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Autophagy, Axons, Cell Survival, Cells, Cultured, Cytoplasm, Disease Models, Animal, Humans, Intermediate Filaments, Motor Neurons, Mutation, Signal Transduction, Mice, Transforming Growth Factor beta1, TOR Serine-Threonine Kinases, Protein Aggregation, Pathological, Protein Aggregates
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