ArticleFrontiers in behavioral neuroscience2023
Enriched environment promotes post-stroke angiogenesis through astrocytic interleukin-17A.
Article in Frontiers in behavioral neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Astrocyte-derived IL-17A facilitates angiogenesis following ischemia-like injury via an IL-6-dependent STAT3-VEGF signaling cascade.Behavioral and brain functions : BBF · 2026Article
- Enriched Environment Suppresses Neuronal Ferroptosis Through SIRT1/AKT/GSK3β-Dependent Glycogen Metabolic Reprogramming After Cerebral Ischemia-Reperfusion.Antioxidants (Basel, Switzerland) · 2026Article
- Clinical value of IL-17-targeted intervention in tissue injury repair: from bidirectional mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- A Scoping Review of Preclinical Environmental Enrichment Protocols in Models of Poststroke to Set the Foundations for Translating the Paradigm to Clinical Settings.Translational stroke research · 2025Article
- Enriched environment inhibits GLT-1 ubiquitination by downregulating SMURF1 to attenuate ischemic brain injury induced excitotoxicity.Cell & bioscience · 2025Article
- CD4Frontiers in immunology · 2025Review
- Astrocyte-Derived Extracellular Vesicles for Ischemic Stroke: Therapeutic Potential and Prospective.Aging and disease · 2024Review
- Th17 Cells and IL-17A in Ischemic Stroke.Molecular neurobiology · 2024Review
- Environmental enrichment enhanced neurogenesis and behavioral recovery after stroke in aged rats.Aging · 2023Article
- Enriched environment-induced neuroplasticity in ischemic stroke and its underlying mechanisms.Frontiers in cellular neuroscience · 2023Review
- Recent advances in tissue repair of the blood-brain barrier after stroke.Journal of tissue engineeringReview
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Our previous studies have revealed that the protective effect of an enriched environment (EE) may be linked with astrocyte proliferation and angiogenesis. However, the relationship between astrocytes and angiogenesis under EE conditions still requires further study. The current research examined the neuroprotective effects of EE on angiogenesis in an astrocytic interleukin-17A (IL-17A)-dependent manner following cerebral ischemia/reperfusion (I/R) injury. Methods: A rat model of ischemic stroke based on middle cerebral artery occlusion (MCAO) for 120 min followed by reperfusion was established, after which rats were housed in either EE or standard conditions. A set of behavior tests were conducted, including the modified neurological severity scores (mNSS) and the rotarod test. The infarct volume was evaluated by means of 2,3,5-Triphenyl tetrazolium chloride (TTC) staining. To evaluate the levels of angiogenesis, the protein levels of CD34 were examined by means of immunofluorescence and western blotting, while the protein and mRNA levels of IL-17A, vascular endothelial growth factor (VEGF), and the angiogenesis-associated factors interleukin-6 (IL-6), JAK2, and STAT3 were detected by western blotting and real-time quantitative PCR (RT-qPCR). Results: We found that EE promoted functional recovery, reduced infarct volume, and enhanced angiogenesis compared to rats in standard conditions. IL-17A expression in astrocytes was also increased in EE rats. EE treatment increased the levels of microvascular density (MVD) and promoted the expression of CD34, VEGF, IL-6, JAK2, and STAT3 in the penumbra, while the intracerebroventricular injection of the IL-17A-neutralizing antibody in EE rats attenuated EE-mediated functional recovery and angiogenesis. Conclusion: Our findings revealed a possible neuroprotective mechanism of astrocytic IL-17A in EE-mediated angiogenesis and functional recovery after I/R injury, which might provide the theoretical basis for EE in clinical practise for stroke patients and open up new ideas for the research on the neural repair mechanism mediated by IL-17A in the recovery phase of stroke.
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