NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Reviewer access | Sign OutHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE59148 Query DataSets for GSE59148
Status Public on Mar 03, 2015
Title The Sarcoglycan complex is expressed in the cerebrovascular system and is specifically regulated by astroglial Cx30 channels
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Summary 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 protein 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 (Cx30Δ/Δ), 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 g-Sarcoglycan (SG), a member of the Dystrophin-associated protein complex (DAPC) connecting cytoskeleton and the extracellular matrix. The same molecular event occurs in Cx30T5M/T5M mutated mice, where Cx30 channels are closed, demonstrating that Sgcg regulation relied on Cx30 channel functions. We further characterized the cerebrovascular Sarcoglycan complex (SGC) and showed the presence of α-, β-, δ-, γ-, ε- and ζ- SG, as well as Sarcospan. Altogether, our results suggest that the Sarcoglycan complex is present in the cerebrovascular system, and that expression of one of its members, g-Sarcoglycan, 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.
 
Overall design Comparison of 3-month-old Cx30 deleted mice against WT genetic background.
 
Contributor(s) Boulay A, Saubaméa B, Cisternino S, Jourdren L, Blugeon C, Cohen-Salmon M
Citation(s) 25698924
Submission date Jul 07, 2014
Last update date May 15, 2019
Contact name Laurent Jourdren
Organization name École Normale Supérieure
Department Biologie
Lab Genomic platform
Street address 46 rue d'Ulm
City Paris
ZIP/Postal code 75230
Country France
 
Platforms (1)
GPL15103 Illumina HiSeq 1000 (Mus musculus)
Samples (3)
GSM1429423 C57BL6_control WT
GSM1429424 C57BL6 Cx30-/-
GSM1563049 C57BL6-BALB/c WT
Relations
BioProject PRJNA254499
SRA SRP044108

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE59148_RAW.tar 5.1 Mb (http)(custom) TAR (of TSV)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap