ArticleProceedings of the National Academy of Sciences of the United States of America2012
β-Catenin signaling initiates the activation of astrocytes and its dysregulation contributes to the pathogenesis of astrocytomas.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
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- Emerging Roles of Adenosine Metabolism in Astrocytes During Brain Injury.CNS neuroscience & therapeutics · 2026Review
- Targeting β-catenin degradation with GSK3β inhibitors induces cell death in acute lymphoblastic leukemia.Nature cancer · 2026Article
- Defective Astrocyte Maturation Drives Cerebellar Neuroinflammation and Degeneration.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Characterizing Microglial Signaling Dynamics During Inflammation Using Single-Cell Mass Cytometry.Glia · 2025Article
- Propofol Protects the Blood-Brain Barrier After Traumatic Brain Injury by Stabilizing the Extracellular Matrix via Prrx1: From Neuroglioma to Neurotrauma.Neurochemical research · 2024Article
- Characterizing microglial signaling dynamics during inflammation using single-cell mass cytometry.bioRxiv : the preprint server for biology · 2024Article
- Canonical Wnt activator Chir99021 prevents epileptogenesis in the intrahippocampal kainate mouse model of temporal lobe epilepsy.Experimental neurology · 2024Article
- A miR-124-mediated post-transcriptional mechanism controlling the cell fate switch of astrocytes to induced neurons.Stem cell reports · 2023Article
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- A lignan from Alnus japonica inhibits glioblastoma tumorspheres by suppression of FOXM1.Scientific reports · 2022Article
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- Reduced Oligodendrocyte Precursor Cell Impairs Astrocytic Development in Early Life Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Urokinase-type plasminogen activator-mediated crosstalk between N-cadherin and β-catenin promotes wound healing.Journal of cell science · 2021Article
- Opposed Interplay between IDH1 Mutations and the WNT/β-Catenin Pathway: Added Information for Glioma Classification.Biomedicines · 2021Review
- Obesity induced by estrogen deficiency is associated with hypothalamic inflammation.Biochemistry and biophysics reports · 2020Article
- Triptolide suppresses IDH1-mutated malignancy via Nrf2-driven glutathione metabolism.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Blockade of Glutathione Metabolism inMolecular cancer therapeutics · 2020Article
- Olanzapine-Induced Activation of Hypothalamic Astrocytes and Toll-Like Receptor-4 Signaling via Endoplasmic Reticulum Stress Were Related to Olanzapine-Induced Weight Gain.Frontiers in neuroscience · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
Astrocytes are the most abundant cell of the CNS and demonstrate contact inhibition in which a nonproliferative, nonmotile cellular state is achieved once stable intercellular contacts are formed between mature cells. Cellular injury disrupts these intercellular contacts, causing a loss of contact inhibition and the rapid initiation of healing. Dysregulation of the molecular pathways involved in this process is thought to lead to an aggressive cellular state associated with neoplasia. We investigated whether a comparable correlation exists between the response of astrocytes to injury and the malignant phenotype of astrocytomas. We discovered that the loss of contact inhibition plays a critical role in the initiation and regulation of reactive astrocytes in the healing of wounds. In particular, injury of the astrocytes interrupts and destabilizes the cadherin-catenin complexes at the cell membrane leading to nuclear translocation of β-catenin and characteristic changes associated with the activation of astrocytes. Similar signaling pathways are found to be active--but dysregulated--in astrocytomas. Inhibition of β-catenin signaling diminished both the response of astrocytes to injury and induction of the malignant phenotype of astrocytomas. The findings shed light on a unique mechanism associated with the pathogenesis of astrocytomas and provide a model for the loss of contact inhibition that may broadly apply to understanding the mechanisms of tissue repair and tumorigenesis in the brain.
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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.