ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Endothelin-1 regulates astrocyte proliferation and reactive gliosis via a JNK/c-Jun signaling pathway.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
What it found
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Who cites it
134 citing papers in PubMed, 244 citations in OpenAlex.
- Human single-cell atlas of proliferative diabetic retinopathy reveals a SOX15-overexpressing stromal population driving retinal fibrosis through the endothelin-1 -EDNRB axis.Journal of translational medicine · 2026Article
- Astrocytes in Multiple Sclerosis: Getting to the Core.International journal of molecular sciences · 2026Review
- Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma.bioRxiv : the preprint server for biology · 2026Article
- Endothelial Netrin-4 regulates oligodendrocyte precursor cell proliferation and differentiation via ET-1 signaling in preterm white matter injury.Brain pathology (Zurich, Switzerland) · 2026Article
- Advances in nano-TCM for Alzheimer's disease: lipid-based carriers integrated with innovative delivery strategies.Journal of nanobiotechnology · 2026Review
- Neurodegeneration Biomarkers in Epilepsy: A Critical Review of Current Findings.Life (Basel, Switzerland) · 2026Review
- Thyroxine Treatment after Traumatic Brain Injury Suppresses Astrogliosis and Enhances Neuronal Recovery in Mice.Thyroid : official journal of the American Thyroid Association · 2025Article
- AAV2-driven endothelin induces chronic reduced retinal blood flow/retinal ganglion cell loss in rats.Life science alliance · 2025Article
- Astrocytic ET-1 System Determines Microglia Phenotype Following Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Microglial cell proliferation is regulated, in part, by reactive astrocyte ETBExperimental neurology · 2025Article
- From Physiology to Pathology of Astrocytes: Highlighting Their Potential as Therapeutic Targets for CNS Injury.Neuroscience bulletin · 2025Review
- Hyperglycemia enhances brain susceptibility to lipopolysaccharide-induced neuroinflammation via astrocyte reprogramming.Journal of neuroinflammation · 2024Article
- Translational Relevance of Secondary Intracellular Signaling Cascades Following Traumatic Spinal Cord Injury.International journal of molecular sciences · 2024Review
- Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.Journal of neuroinflammation · 2024Article
- Review
- Combination of blockade of endothelin signalling and compensation of IGF1 expression protects the retina from degeneration.Cellular and molecular life sciences : CMLS · 2024Article
- Astrocyte-Neuron Interactions Contributing to Amyotrophic Lateral Sclerosis Progression.Advances in neurobiology · 2024Review
- Activation of Neurotoxic Astrocytes Due to Mitochondrial Dysfunction Triggered byInternational journal of biological sciences · 2024Article
- Article
- The Tetraspanin Tspan8 Associates with Endothelin Converting Enzyme ECE1 and Regulates Its Activity.Cancers · 2023Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Reactive gliosis is characterized by enhanced glial fibrillary acidic protein (GFAP) expression, cellular hypertrophy, and astrocyte proliferation. The cellular and molecular mechanisms underlying this process are still largely undefined. We investigated the role of endothelin-1 (ET-1) in reactive gliosis in corpus callosum after lysolecithin (LPC)-induced focal demyelination and in cultured astrocytes. We show that ET-1 levels are upregulated in demyelinated lesions within 5 d after LPC injection, together with enhanced astrocyte proliferation, GFAP expression, and JNK phosphorylation. Infusion of the pan-ET-receptor (ET-R) antagonist Bosentan or the selective ET(B)-R antagonist BQ788 into the corpus callosum prevented postlesion astrocyte proliferation and JNK phosphorylation. In cultured astrocytes, ET-1-induced activation of ET(B)-Rs promotes a reactive phenotype by enhancing both GFAP expression and astrocyte proliferation. In the same cells, ET-1 activates both JNK and p38MAPK pathways, and induces c-Jun expression at the mRNA and protein levels. By using selective pharmacological inhibitors, we also provide evidence that ET-1 induces astrocyte proliferation and GFAP expression through activation of ERK- and JNK-dependent pathways, consistent with the previous observation of ET-1-induced activation of ERK (Schinelli et al., 2001). Finally, we show by gain and loss of function that increased c-Jun expression enhances the proliferative response of astrocytes to ET-1, whereas c-jun siRNA prevents ET-1-induced cell proliferation. Our results indicate that the effects of ET-1 on astrocyte proliferation depend on c-Jun induction and activation through ERK- and JNK-dependent pathways, and suggest that ET-R-associated pathways might represent important targets to control reactive gliosis.
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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.