ArticleNeurochemical research2011
Nogo-66 inhibits the dye-coupling of astrocytic gap junctions in vitro.
Article in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- Gap junction communication in myelinating glia.Biochimica et biophysica acta · 2013Review
- Distinct roles of Nogo-a and Nogo receptor 1 in the homeostatic regulation of adult neural stem cell function and neuroblast migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
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5 authors at 2 institutions in 1 country.
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Abstract
Communication between astrocytes via the gap junction is crucial for maintaining homeostasis of the extra-neuronal microenvironment of the central nervous system. Dysfunction of astrocytic gap junctions is involved in many brain disorders. Our previous studies demonstrated a novel co-localization of Nogo-66 receptor at glial gap junctions in rat cerebellum and posterior pituitary. The present study was aimed at exploring whether Nogo-66 can modulate glial gap junctions in vitro. We confirmed the co-localization of Nogo-66 receptor with Cx43 in cultured astrocytes, and stimulated astrocytes with myelin extracts, or Nogo-66-Fc conditioned medium. Finally, we expressed and purified a functionally effective GST-Nogo-66 peptide. Lucifer yellow transfer assay was adopted to measure the gap junction permeability. The results showed that the spreading of Lucifer yellow was inhibited significantly by all three treatments as compared with their corresponding controls. Therefore, this study shows a novel inhibitory effect of Nogo-66 on the permeability of astrocytic gap junctions, suggesting a presumable role of Nogo-66 receptor in modulating the glial gap junction.
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