
Segment‐specific but pathologic laminin isoform profiles in human labial salivary glands of patients with Sjögren's syndrome
Author(s) -
Laine Mikael,
Virtanen Ismo,
Salo Tuula,
Konttinen Yrjö T.
Publication year - 2004
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.20730
Subject(s) - laminin , basement membrane , myoepithelial cell , extracellular matrix , biology , immunohistochemistry , pathology , chemistry , microbiology and biotechnology , medicine , immunology
Objective To assess the laminins in basement membrane of the labial salivary glands of patients with Sjögren's syndrome (SS) and healthy controls. Methods Labeling of laminin α1–α5, β1, β2, γ1, and γ2 chains was performed using immunohistochemistry with chain‐specific monoclonal antibodies and pattern recognition analysis of the labeled specimens. Results Laminin α1, α2, and α4 chains were detected exclusively in the acinar basement membranes, whereas laminin α3, α5, β1, γ1, and γ2 chains were also detected in ductal basement membranes. Laminin β2 chain was not found. In patients with SS, laminin α1 and α2 chains were weakly labeled, but laminin α4 labeling was also intense in areas not infiltrated by lymphocytes. Pattern recognition analysis suggested that laminin α1, α2, and α4 chains were associated with acinar cells, myoepithelial cells, and tissue damage/repair, respectively. Conclusion All salivary gland basement membranes signal through laminin 5, laminin 6, and laminin 10 trimers, but acinar basement membranes also signal through laminin 1, laminin 2, and laminin 8 trimers. Laminin α1 chain/laminin 1 may play a central role in the maintenance of acinar cells in healthy glands. This possibility was supported by the finding of variable expression of laminin α1 chain/laminin 1 in acinar basement membrane and its weak expression in SS with acinar cell atrophy. The impairment of myoepithelial laminin α2 chain/laminin 2 in patients with SS indicates a double defect in the acinar compartment and pathologic extracellular matrix–to‐cell signaling, which may contribute to structural deterioration and functional abnormality of the exocrine glands.