ArticleFrontiers in cellular neuroscience2015
The Sarcoglycan complex is expressed in the cerebrovascular system and is specifically regulated by astroglial Cx30 channels.
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 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Genome-wide association analyses of borderline personality disorder identify 11 loci and highlight shared risk with mental and somatic disorders.Nature genetics · 2026Pooled it
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- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Expression of Dystrophin Dp71 Splice Variants Is Temporally Regulated During Rodent Brain Development.Molecular neurobiology · 2024Article
- The role of astrocytes in the glymphatic network: a narrative review.Metabolic brain disease · 2024Review
- Alternative Splicing Changes Promoted by NOVA2 Upregulation in Endothelial Cells and Relevance for Gastric Cancer.International journal of molecular sciences · 2023Article
- Connexins Signatures of the Neurovascular Unit and Their Physio-Pathological Functions.International journal of molecular sciences · 2022Review
- Proteomics and Transcriptomics of the Hippocampus and Cortex in SUDEP and High-Risk SUDEP Patients.Neurology · 2021Article
- Muscle Diversity, Heterogeneity, and Gradients: Learning from Sarcoglycanopathies.International journal of molecular sciences · 2021Review
- Cellular mechanisms and molecular signaling pathways in stress-induced anxiety, depression, and blood-brain barrier inflammation and leakage.Inflammopharmacology · 2020Review
- Modulating the water channel AQP4 alters miRNA expression, astrocyte connectivity and water diffusion in the rodent brain.Scientific reports · 2018Article
- A transcriptome-based assessment of the astrocytic dystrophin-associated complex in the developing human brain.Journal of neuroscience research · 2018Article
- Function of Connexins in the Interaction between Glial and Vascular Cells in the Central Nervous System and Related Neurological Diseases.Neural plasticity · 2018Review
- Connexin Channels at the Glio-Vascular Interface: Gatekeepers of the Brain.Neurochemical research · 2017Review
- Update on the Genetics of Dystonia.Current neurology and neuroscience reports · 2017Review
- Myoclonus dystonia and muscular dystrophy: ɛ-sarcoglycan is part of the dystrophin-associated protein complex in brain.Movement disorders : official journal of the Movement Disorder Society · 2016Article
- Purification of Mouse Brain Vessels.Journal of visualized experiments : JoVE · 2015Article
- Connexin and pannexin signaling pathways, an architectural blueprint for CNS physiology and pathology?Cellular and molecular life sciences : CMLS · 2015Review
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8 authors.
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Abstract
Astrocytes, the most prominent glial cell type in the brain, send specialized processes called endfeet, around blood vessels and express a large molecular repertoire regulating the cerebrovascular system physiology. One of the most striking properties of astrocyte endfeet is their enrichment in gap junction proteins Connexin 43 and 30 (Cx43 and Cx30) allowing in particular for direct intercellular trafficking of ions and small signaling molecules through perivascular astroglial networks. In this study, we addressed the specific role of Cx30 at the gliovascular interface. Using an inactivation mouse model for Cx30 (Cx30(Δ/Δ); Δ means deleted allele) we showed that absence of Cx30 does not affect blood-brain barrier (BBB) organization and permeability. However, it results in the cerebrovascular fraction, in a strong upregulation of Sgcg encoding γ-Sarcoglycan (γ-SG), a member of the Dystrophin-associated protein complex (DAPC) connecting cytoskeleton and the extracellular matrix. The same molecular event occurs in Cx30(T5M/T5M) mutated mice, where Cx30 channels are closed, demonstrating that Sgcg regulation relied on Cx30 channel functions. We further characterized the expression of other Sarcoglycan complex (SGC) molecules in the cerebrovascular system and showed the presence of α-, β-, δ-, γ-, ε- and ζ- SG, as well as Sarcospan. Their expression was however not modified in Cx30(Δ/Δ). These results suggest that a full SGC might be present in the cerebrovascular system, and that expression of one of its member, γ-SG, depends on Cx30 channels. As described in skeletal muscles, the SGC may contribute to membrane stabilization and signal transduction in the cerebrovascular system, which may therefore be regulated by Cx30 channel-mediated functions.
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