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The Journal of Neuroscience, 0000, 20:RC114:1-6
RAPID COMMUNICATION
Reciprocal Regulation of the Junctional Proteins Claudin-1 and
Connexin43 by Interleukin-1 in Primary Human Fetal Astrocytes
Heather S.
Duffy1,
Gareth R.
John2,
Sunhee C.
Lee2,
Celia F.
Brosnan1, 2, and
David C.
Spray1
Departments of 1 Neuroscience and
2 Pathology, Albert Einstein College of Medicine, Bronx,
New York 10461
Vertebrate tissues use multiple junctional types to establish and
maintain tissue architecture, including gap junctions for cytoplasmic
connectivity and tight junctions (TJs) for paracellular and/or cell
polarity barriers. The integral membrane proteins of gap junctions are
connexins, whereas TJs are a complex between occludin and members of a
recently characterized multigene family, the claudins. In normal brain,
astrocytes are coupled by gap junctions composed primarily of
connexin43 (Cx43), whereas TJs have not been detected in these cells.
We now show that treatment of primary human astrocytes with the
cytokine interleukin-1 (IL-1) causes rapid induction of
claudin-1, with an expression pattern reciprocal to loss of Cx43.
Treatment also led to protracted downregulation of occludin but no
change in expression of zonula occludens proteins ZO-1 and -2. Immunofluorescence staining localized claudin-1 to cell membranes in
IL-1-treated astrocytes, whereas freeze-fracture replicas showed
strand-like arrays of intramembranous particles in treated cells
resembling rudimentary TJ assemblies. We conclude that in human
astrocytes, IL-1 regulates expression of the claudin multigene
family and that gap and tight junction proteins are inversely regulated
by this proinflammatory cytokine. We suggest that in pathological
conditions of the human CNS, elevated IL-1 expression fundamentally
alters astrocyte-to-astrocyte connectivity.
Key words:
gap junction; tight junction; cytokine; astrocyte; CNS; human
Copyright © 0000 Society for Neuroscience 0270-6474/00/$05.00/0
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