ArticleFrontiers in cellular neuroscience2015
Dystroglycan controls dendritic morphogenesis of hippocampal neurons in vitro.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- The cell adhesion protein dystroglycan affects the structural remodeling of dendritic spines.Scientific reports · 2022Article
- Connecting the Neurobiology of Developmental Brain Injury: Neuronal Arborisation as a Regulator of Dysfunction and Potential Therapeutic Target.International journal of molecular sciences · 2021Review
- Quantification of Dendritic Spines Remodeling under Physiological Stimuli and in Pathological Conditions.International journal of molecular sciences · 2021Review
- Review
- Serotonin 5-HTCommunications biology · 2020Article
- Arhgef5 Binds α-Dystrobrevin 1 and Regulates Neuromuscular Junction Integrity.Frontiers in molecular neuroscience · 2020Article
- Recent advances in branching mechanisms underlying neuronal morphogenesis.F1000Research · 2018Review
- Matrix Metalloproteinase 9 in Epilepsy: The Role of Neuroinflammation in Seizure Development.Mediators of inflammation · 2016Review
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Dendritic outgrowth and arborization are important for establishing neural circuit formation. To date, little information exists about the involvement of the extracellular matrix (ECM) and its cellular receptors in these processes. In our studies, we focus on the role of dystroglycan (DG), a cell adhesion molecule that links ECM components to the actin cytoskeleton, in dendritic development and branching. Using a lentiviral vector to deliver short-hairpin RNA (shRNA) that specifically silences DG in cultured hippocampal neurons, we found that DG knockdown exerted an inhibitory effect on dendritic tree growth and arborization. The structural changes were associated with activation of the guanosine triphosphatase Cdc42. The overexpression of DG promoted dendritic length and branching. Furthermore, exposure of the cultures to autoactivating matrix metalloproteinase-9 (aaMMP-9), a β-DG-cleaving protease, decreased the complexity of dendritic arbors. This effect was abolished in neurons that overexpressed a β-DG mutant that was defective in MMP-9-mediated cleavage. Altogether, our results indicate that DG controls dendritic arborization in vitro in MMP-9-dependent manner.
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