The JAK/STAT3 pathway is a common inducer of astrocyte reactivity in Alzheimer’s and Huntington’s diseases
Open accessAbstract
Astrocyte reactivity is a hallmark of neurodegenerative diseases (ND), but its effects on disease outcomes remain highly debated. Elucidation of the signaling cascades inducing reactivity in astrocytes during ND would help characterize the function of these cells and identify novel molecular targets to modulate disease progression. The Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway is associated with reactive astrocytes in models of acute injury, but it is unknown whether this pathway is directly responsible for astrocyte reactivity in progressive pathological conditions such as ND. In this study, we examined whether the JAK/STAT3 pathway promotes astrocyte reactivity in several animal models of ND. The JAK/STAT3 pathway was activated in reactive astrocytes in two transgenic mouse models of Alzheimer's disease and in a mouse and a nonhuman primate lentiviral vector-based model of Huntington's disease (HD). To determine whether this cascade was instrumental for astrocyte reactivity, we used a lentiviral vector that specifically targets astrocytes in vivo to overexpress the endogenous inhibitor of the JAK/STAT3 pathway [suppressor of cytokine signaling 3 (SOCS3)]. SOCS3 significantly inhibited this pathway in astrocytes, prevented astrocyte reactivity, and decreased microglial activation in models of both diseases. Inhibition of the JAK/STAT3 pathway within reactive astrocytes also increased the number of huntingtin aggregates, a neuropathological hallmark of HD, but did not influence neuronal death. Our data demonstrate that the JAK/STAT3 pathway is a common mediator of astrocyte reactivity that is highly conserved between disease states, species, and brain regions. This universal signaling cascade represents a potent target to study the role of reactive astrocytes in ND.
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The STAT3 pathway is elevated in reactive astrocytes of Aβ mouse models.
“the STAT3 pathway is shown to be elevated in reactive astrocytes of Aβ mouse models”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Ben Haim et al., 2015
In Aβ mouse models, SOCS3 expression effectively reduced reactive astrogliosis and microgliosis.
“where the expression of SOCS3 effectively reduced reactive astrogliosis and microgliosis (Ben Haim et al., 2015).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Ben Haim et al., 2015
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- Authors
- Ben Haim, L., Ceyzériat, K., Carrillo-de Sauvage, M. A., Aubry, F., Auregan, G., Guillermier, M., Ruiz, M., Petit, F., Houitte, D., Faivre, E., Vandesquille, M., Aron-Badin, R., Dhenain, M., Déglon, N., Hantraye, P., Brouillet, E., Bonvento, G., & Escartin, C.
- Affiliations
- Université Paris-Sud (FR)
- ORCID
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2015-02-11
- Volume
- 35
- Issue
- 6
- Pages
- 2817-2829
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6605603
- OpenAlex
- W1993573917
- Cited by
- 335
- References
- 60
- Citations by year
- 2026: 38 · 2025: 40 · 2024: 37 · 2023: 27 · 2022: 31 · 2021: 38 · 2020: 37 · 2019: 27 · 2018: 23 · 2017: 20 · 2016: 11 · 2015: 6
- FWCI
- 10.69
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, other-oa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- SERVAL (Université de Lausanne) (publishedVersion, other-oa)
- HAL (submittedVersion, other-oa)
- Funders
- Agence Nationale de la Recherche (ANR-11-INBS-0011)
- Association France Alzheimer
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- JAK/STAT3 signaling, astrocyte activation, Alzheimer's disease, Huntington's disease, neurodegenerative diseases, SOCS3, microglial activation, huntingtin aggregates, transgenic mouse model, nonhuman primate model
- MeSH terms
- Suppressor of Cytokine Signaling 3 Protein, Alzheimer Disease, Animals, Astrocytes, Electron Transport Complex IV, Humans, Huntington Disease, Macaca fascicularis, Male, Mice, Inbred C57BL, Mice, Transgenic, Signal Transduction, NF-kappa B, Serotonin Plasma Membrane Transport Proteins, STAT3 Transcription Factor, Suppressor of Cytokine Signaling Proteins, Mice, Janus Kinases
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Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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