ArticleProceedings of the National Academy of Sciences of the United States of America2013
Calcium-dependent N-cadherin up-regulation mediates reactive astrogliosis and neuroprotection after brain injury.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 1 of them a synthesis that pooled it.
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Who cites it
74 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- Neurotransmission-related gene expression in the frontal pole is altered in subjects with bipolar disorder and schizophrenia.Translational psychiatry · 2023Pooled it
- Altered astrocyte-neuron crosstalk in progressive supranuclear palsy: integrated evidence from proteomics and magnetic resonance spectroscopy.Acta neuropathologica · 2026Article
- Knockout of Low-Density Lipoprotein Receptor-Related Protein 1 From Astrocytes in Adult Mice Accelerates Long-Term Functional Recovery After Ischemic Stroke.Brain and behavior · 2026Article
- Calcium Signaling in Astrocytes and Its Role in the Central Nervous System Injury.Molecular neurobiology · 2025Review
- New therapeutic approaches for fibrosis: harnessing translational regulation.Trends in molecular medicine · 2025Review
- Wnt/β-catenin Pathway Aggravates Renal Fibrosis by Activating PUM2 Transcription to Repress YME1L-mediated Mitochondrial Homeostasis.Biochemical genetics · 2025Article
- Melatonin ameliorates astrogliosis and microgliosis in a cuprizone demyelinating mouse model.Biochemistry and biophysics reports · 2025Article
- (Re)building the nervous system: A review of neuron-glia interactions from development to disease.Journal of neurochemistry · 2025Review
- Invasive growth of brain metastases is linked to CHI3L1 release from pSTAT3-positive astrocytes.Neuro-oncology · 2024Article
- Activation of Neurotoxic Astrocytes Due to Mitochondrial Dysfunction Triggered byInternational journal of biological sciences · 2024Article
- Article
- Genetic Ablation of Inositol 1,4,5-Trisphosphate Receptor Type 2 (IPInternational journal of molecular sciences · 2023Article
- Neuroprotective astroglial response to neural damage and its relevance to affective disorders.Exploration of neuroprotective therapy · 2023Article
- Tackling the glial scar in spinal cord regeneration: new discoveries and future directions.Frontiers in cellular neuroscience · 2023Review
- Paxillin tunes the relationship between cell-matrix and cell-cell adhesions to regulate stiffness-dependent dentinogenesis.Regenerative biomaterials · 2023Article
- Hypothalamic astrocytes control systemic glucose metabolism and energy balance.Cell metabolism · 2022Article
- Generation of Human iPSC-Derived Astrocytes with a mature star-shaped phenotype for CNS modeling.Stem cell reviews and reports · 2022Article
- Calcium acts as a central player in melatonin antitumor activity in sarcoma cells.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Calcium signaling in individual APP/PS1 mouse dentate gyrus astrocytes increases ex vivo with Aβ pathology and age without affecting astrocyte network activity.Journal of neuroscience research · 2022Article
- Bridging the gap of axonal regeneration in the central nervous system: A state of the art review on central axonal regeneration.Frontiers in neuroscience · 2022Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain injury induces phenotypic changes in astrocytes, known as reactive astrogliosis, which may influence neuronal survival. Here we show that brain injury induces inositol 1,4,5-trisphosphate (IP3)-dependent Ca(2+) signaling in astrocytes, and that the Ca(2+) signaling is required for astrogliosis. We found that type 2 IP3 receptor knockout (IP3R2KO) mice deficient in astrocytic Ca(2+) signaling have impaired reactive astrogliosis and increased injury-associated neuronal death. We identified N-cadherin and pumilio 2 (Pum2) as downstream signaling molecules, and found that brain injury induces up-regulation of N-cadherin around the injured site. This effect is mediated by Ca(2+)-dependent down-regulation of Pum2, which in turn attenuates Pum2-dependent translational repression of N-cadherin. Furthermore, we show that astrocyte-specific knockout of N-cadherin results in impairment of astrogliosis and neuroprotection. Thus, astrocytic Ca(2+) signaling and the downstream function of N-cadherin play indispensable roles in the cellular responses to brain injury. These findings define a previously unreported signaling axis required for reactive astrogliosis and neuroprotection following brain injury.
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