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IMMUNOCYTOCHEMICAL EVIDENCE FOR A MODULATION OF GALECTIN 3 (Mac‐2), A CARBOHYDRATE BINDING PROTEIN, IN PULMONARY FIBROSIS
Author(s) -
KASPER MICHAEL,
HUGHES R. COLIN
Publication year - 1996
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199607)179:3<309::aid-path572>3.0.co;2-d
Subject(s) - galectin 3 , galectin , modulation (music) , galectin 1 , carbohydrate , pulmonary fibrosis , chemistry , fibrosis , microbiology and biotechnology , medicine , biology , biochemistry , physics , acoustics
Galectin 3 is an endogenous mammalian carbohydrate‐binding protein with affinity for terminal β‐galactose residues, polylactosamine glycans, and ABH‐blood group carbohydrate epitopes. To determine the distribution and regulation of galectin 3 during pulmonary injury, which is known to be accompanied by profound changes in the carbohydrate moieties of cell surface glycoproteins of alveolar cells, a rat model of irradiation‐induced lung inflammation and repair was used. Immunocytochemistry showed that in normal rat lungs, galectin 3 was localized to alveolar macrophages, with weaker staining of bronchial epithelial cells. Shortly after irradiation‐induced lung injury, when there is active proliferation of type II alveolar epithelial cells and re‐epithelialization of alveolar basement membranes by type I cells, the total galectin concentration in the lung increased dramatically. This increase was due in part to an increased population of galectin 3‐positive interstitial and alveolar macrophages. In addition, galectin 3 was expressed prominently at the surface of the newly formed type I alveolar epithelium and to lesser extent at the apical surface of type II cells. These findings suggest that the increased synthesis and secretion of galectin 3 during irradiation‐induced lung injury, together with ligation of secreted lectin at the surface of alveolar epithelial cells, may play roles in pulmonary alveolar epithelial expansion and differentiation during injury and repair.