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Connective tissue diseases

Does mucin about cause acinar defects?

Nature Reviews Rheumatology volume 8, page 186 (2012)Cite this article

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“Patients with Sjögren's syndrome have disturbances in tight junctions and hemidesmosomes,” explains González. Cell–cell and cell–ECM interactions involving these structures determine cell polarity and compartmentalization, and this organization is essential for normal exocytosis; therefore, defective exocytosis might be at least partially responsible for acinar cell and exocrine gland dysfunction in Sjögren's syndrome. This hypothesis “led us to study the expression and localization of SNARE fusion receptors present in secretory granules (VAMP8 and STX3) and the plasma membrane (STX4 and SNAP23),” says González.

Their investigations revealed increased complex formation between the SNARE proteins in acinar cells derived from patients with Sjögren's syndrome, compared with cells from healthy control individuals. “Formation of high levels of these SNARE complexes in Sjögren's syndrome suggests probable supraphysiological stimulation of regulated exocytosis.” Furthermore, the proteins were aberrantly expressed, and relocalized from a predominantly apical distribution in control cells to a more basal location in Sjögren's syndrome acini.

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ORIGINAL RESEARCH PAPER

  1. Barrera, M. J. et al. Aberrant localization of fusion receptors involved in regulated exocytosis in salivary glands of Sjögren's syndrome patients is linked to ectopic mucin secretion. J. Autoimmunity doi:10.1016/j.jaut.2012.01.011.

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  1. David Killock
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Killock, D. Does mucin about cause acinar defects?. Nat Rev Rheumatol 8, 186 (2012). https://doi.org/10.1038/nrrheum.2012.20

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  • DOI: https://doi.org/10.1038/nrrheum.2012.20

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