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免疫细胞化学证据表明,在肺纤维化中,一种碳水化合物结合蛋白——半乳糖凝集素3(Mac-2)受到了调节。

Immunocytochemical evidence for a modulation of galectin 3 (Mac-2), a carbohydrate binding protein, in pulmonary fibrosis.

作者信息

Kasper M, Hughes R C

机构信息

Institute of Pathology, Technical University of Dresden, Germany.

出版信息

J Pathol. 1996 Jul;179(3):309-16. doi: 10.1002/(SICI)1096-9896(199607)179:3<309::AID-PATH572>3.0.CO;2-D.

DOI:10.1002/(SICI)1096-9896(199607)179:3<309::AID-PATH572>3.0.CO;2-D
PMID:8774488
Abstract

Galectin 3 is endogenous mammalian carbohydrate-binding protein with affinity for terminal beta-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.

摘要

半乳糖凝集素-3是一种内源性哺乳动物碳水化合物结合蛋白,对末端β-半乳糖残基、多乳糖胺聚糖和ABH血型碳水化合物表位具有亲和力。为了确定半乳糖凝集素-3在肺损伤过程中的分布和调节情况(已知肺损伤伴随着肺泡细胞表面糖蛋白碳水化合物部分的深刻变化),使用了辐射诱导的肺部炎症和修复大鼠模型。免疫细胞化学显示,在正常大鼠肺中,半乳糖凝集素-3定位于肺泡巨噬细胞,支气管上皮细胞染色较弱。辐射诱导的肺损伤后不久,当II型肺泡上皮细胞活跃增殖且I型细胞使肺泡基底膜重新上皮化时,肺中半乳糖凝集素的总浓度急剧增加。这种增加部分归因于半乳糖凝集素-3阳性间质和肺泡巨噬细胞数量的增加。此外,半乳糖凝集素-3在新形成的I型肺泡上皮表面显著表达,在II型细胞的顶端表面表达较少。这些发现表明,辐射诱导的肺损伤过程中半乳糖凝集素-3合成和分泌的增加,以及分泌的凝集素在肺泡上皮细胞表面的结合,可能在损伤和修复过程中肺泡上皮的扩张和分化中发挥作用。

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