ArticleGlia2014
Astrocytic transforming growth factor-beta signaling reduces subacute neuroinflammation after stroke in mice.
Article in Glia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 203 citations in OpenAlex.
- Systematic Review of the Differential Effects of TGF-β1 in Ischemic and Hemorrhagic Preclinical Stroke Models.Journal of the American Heart Association · 2025Pooled it
- Bibliometric and visual analysis of spinal cord injury-associated macrophages from 2002 to 2023.Frontiers in neurology · 2023Pooled it
- Article
- Engineering RVG-modified exosomes for targeting TGF-β1 signaling in stroke recovery.Journal of translational medicine · 2026Article
- Cognitive impairment and prefrontal TGF-β1 elevation in a rat model of fatigue.Frontiers in psychiatry · 2026Article
- Causal relationship between inflammatory cytokines and posttraumatic stress disorder: a Mendelian randomization study and potential mechanism analysis.European journal of psychotraumatology · 2025Article
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- Gosha-Jinki-Gan Reduces Inflammation in Chronic Ischemic Stroke Mouse Models by Suppressing the Infiltration of Macrophages.Biomolecules · 2025Article
- TGFα controls checkpoints in CNS resident and infiltrating immune cells to promote resolution of inflammation.Nature communications · 2025Article
- Semaglultide targets Spp1Journal of neuroinflammation · 2025Article
- Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025Review
- Exploring neuroglial signaling: diversity of molecules implicated in microglia-to-astrocyte neuroimmune communication.Reviews in the neurosciences · 2025Review
- Astrocyte-microglia crosstalk in subarachnoid hemorrhage: mechanisms and treatments.Frontiers in immunology · 2025Review
- Brain border-derived CXCL2CNS neuroscience & therapeutics · 2024Article
- Perioperative stroke deteriorates white matter integrity by enhancing cytotoxic CD8CNS neuroscience & therapeutics · 2024Article
- Astrocytes in functional recovery following central nervous system injuries.The Journal of physiology · 2024Review
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- Stroke Related Brain-Heart Crosstalk: Pathophysiology, Clinical Implications, and Underlying Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Astrocytic Extracellular Vesicles Regulated by Microglial Inflammatory Responses Improve Stroke Recovery.Molecular neurobiology · 2024Article
- Article
67 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Astrocytes limit inflammation after CNS injury, at least partially by physically containing it within an astrocytic scar at the injury border. We report here that astrocytic transforming growth factor-beta (TGFβ) signaling is a second, distinct mechanism that astrocytes utilize to limit neuroinflammation. TGFβs are anti-inflammatory and neuroprotective cytokines that are upregulated subacutely after stroke, during a clinically accessible time window. We have previously demonstrated that TGFβs signal to astrocytes, neurons and microglia in the stroke border days after stroke. To investigate whether TGFβ affects astrocyte immunoregulatory functions, we engineered "Ast-Tbr2DN" mice where TGFβ signaling is inhibited specifically in astrocytes. Despite having a similar infarct size to wildtype controls, Ast-Tbr2DN mice exhibited significantly more neuroinflammation during the subacute period after distal middle cerebral occlusion (dMCAO) stroke. The peri-infarct cortex of Ast-Tbr2DN mice contained over 60% more activated CD11b(+) monocytic cells and twice as much immunostaining for the activated microglia and macrophage marker CD68 than controls. Astrocytic scarring was not altered in Ast-Tbr2DN mice. However, Ast-Tbr2DN mice were unable to upregulate TGF-β1 and its activator thrombospondin-1 2 days after dMCAO. As a result, the normal upregulation of peri-infarct TGFβ signaling was blunted in Ast-Tbr2DN mice. In this setting of lower TGFβ signaling and excessive neuroinflammation, we observed worse motor outcomes and late infarct expansion after photothrombotic motor cortex stroke. Taken together, these data demonstrate that TGFβ signaling is a molecular mechanism by which astrocytes limit neuroinflammation, activate TGFβ in the peri-infarct cortex and preserve brain function during the subacute period after stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.