ArticleBrain communications2019
Activation of both transforming growth factor-β and bone morphogenetic protein signalling pathways upon traumatic brain injury restrains pro-inflammatory and boosts tissue reparatory responses of reactive astrocytes and microglia.
Article in Brain communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
- Suppression of astrocyte BMP signaling improves molecular signatures and functional deficits in a fragile X syndrome mouse model.Nature communications · 2026Article
- Controlled release of bone morphogenetic protein-2 improves motor function after traumatic brain injury in a rat model.Journal of materials chemistry. B · 2026Article
- Dual-peptide engineered macrophage membrane biomimetic nanosystem via targeting Rg1 delivery for traumatic brain injury therapy.Regenerative biomaterials · 2026Article
- Astrocyte activation persists one year after TBI: a dynamic shift from inflammation to neurodegeneration.Communications biology · 2025Article
- Exploring potential targets and molecular mechanisms of traumatic brain injury exacerbated by Benzo(a)pyrene via network toxicology and molecular dynamics simulation.Cell biology and toxicology · 2025Article
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- TGF-β signaling regulates gene expression, phagocytosis, and cell proliferation and supports glial cell survival in primary rat mixed glial cell cultures.Journal of molecular histology · 2025Article
- Extracellular vesicles as biomarkers for traumatic brain injury using a 3D in vitro human brain tissue model.Scientific reports · 2025Article
- Peripheral Blood-Derived Mesenchymal Stem Cells Promote A2 Phenotype Polarization in Astrocytes via TGF-β-Mediated PI3K/Akt Pathway Activation.European journal of medical research · 2025Article
- Transcriptomic analysis reveals shared deregulated neutrophil responses in COVID-19 and idiopathic pulmonary fibrosis.Respiratory research · 2025Article
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- Exosome-shuttled miR-5121 from A2 astrocytes promotes BSCB repair after traumatic SCI by activating autophagy in vascular endothelial cells.Journal of nanobiotechnology · 2025Article
- Administration of Noggin Suppresses Fibrinogen Leakage into the Brain in the Acute Phase After Traumatic Brain Injury in Mice.International journal of molecular sciences · 2025Article
- Exploring Azithromycin's Neuroprotective Role in Traumatic Brain Injury: Insights into Cognitive and Motor Recovery and Neuroinflammatory Modulation.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Vincristine Regulates C/EBP-β/TGF-β1 to Promote A1 Astrocyte Polarization and Induce Neuropathic Pain.Drug design, development and therapy · 2025Article
- Research Trends and Evolution of Astrocytes in Depression and Antidepressant Treatment: A Bibliometric Analysis.Current neuropharmacology · 2025Article
- TGF-β Signaling in Microglia: A Key Regulator of Development, Homeostasis and Reactivity.Biomedicines · 2024Review
- Review
- Astroglial Cells: Emerging Therapeutic Targets in the Management of Traumatic Brain Injury.Cells · 2024Review
- Neutrophil-derived Activin-A moderates their pro-NETotic activity and attenuates collateral tissue damage caused by Influenza A virus infection.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various ligands and receptors of the transforming growth factor-β superfamily have been found upregulated following traumatic brain injury; however, the role of this signalling system in brain injury pathophysiology is not fully characterized. To address this, we utilized an acute stab wound brain injury model to demonstrate that hallmarks of transforming growth factor-β superfamily system activation, such as levels of phosphorylated Smads, ligands and target genes for both transforming growth factor-β and bone morphogenetic protein pathways, were upregulated within injured tissues. Using a bone morphogenetic protein-responsive reporter mouse model, we showed that activation of the bone morphogenetic protein signalling pathway involves primarily astrocytes that demarcate the wound area. Insights regarding the potential role of transforming growth factor-β superfamily activation in glia cells within the injured tissues were obtained indirectly by treating purified reactive astrocytes and microglia with bone morphogenetic protein-4 or transforming growth factor-β1 and characterizing changes in their transcriptional profiles. Astrocytes responded to both ligands with considerably overlapping profiles, whereas, microglia responded selectively to transforming growth factor-β1. Novel pathways, crucial for repair of tissue-injury and blood-brain barrier, such as activation of cholesterol biosynthesis and transport, production of axonal guidance and extracellular matrix components were upregulated by transforming growth factor-β1 and/or bone morphogenetic protein-4 in astrocytes. Moreover, both ligands in astrocytes and transforming growth factor-β1 in microglia shifted the phenotype of reactive glia cells towards the anti-inflammatory and tissue reparatory 'A2'-like and 'M0/M2'-like phenotypes, respectively. Increased expression of selected key components of the
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