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首页> 外文期刊>American Journal of Dermatopathology >Galectin-1 and Galectin-3 and Their Potential Binding Partners in the Dermal Thickening of Keloid Tissues
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Galectin-1 and Galectin-3 and Their Potential Binding Partners in the Dermal Thickening of Keloid Tissues

机译：Galectin-1和Galectin-3及其在瘢痕疙瘩组织的皮肤增厚中的潜在结合伴侣

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Keloids are defined histopathologically as an inflammatory disorder characterized by exhibiting numerous fibroblasts, abnormal vascularization, increased number of proinflammatoty immune cells as well as uncontrolled cell proliferation, and exacerbated and disorganized deposition of extracellular matrix (ECM) molecules. Importantly, many of these ECM molecules display N- and O-linked glycan residues and are considered as potential targets for galectin-1 (Gal-1) and galectin-3 (Gal-3). Nevertheless, the presence and localization of Gal-1 and Gal-3 as well as the interactions with some of their binding partners in keloid tissues have not been considered. Here, we show that in the dermal thickening of keloids, versican, syndecan-1, fibronectin, thrombospondin-1, tenascin C, CD44, integrin beta(1), and N-cadherin were immunolocalized in the elongated fibroblasts that were close to the immune cell infiltrate, attached to collagen bundles, and around the microvasculature and in some immune cells. We also show that Gal-1 and Gal-3 were present in the cytoplasm and along the cell membrane of some fibroblasts and immune and endothelial cells of the dermal thickening. We suggest that Gal-1 and Gal-3, in concert with some of the ECM molecules produced by fibroblasts and by immune cells, counteract the inflammatory response in keloids. We also proposed that Gal-1 and Gal-3 through their binding partners may form a supramolecular structure at the cell surface of fibroblasts, immune cells, endothelial cells, and in the extracellular space that might influence the fibroblast morphology, adhesion, proliferation, migration, and survival as well as the inflammatory responses.
机译：瘢痕疙瘩是组织病理学上定义的，作为炎性疾病，其特征在于表现出许多成纤维细胞，异常血管化，促胰管的免疫细胞数量增加，以及不受控制的细胞增殖，以及细胞外基质（ECM）分子的加剧和混乱沉积。重要的是，许多这些ECM分子显示N-和O型聚糖残基，并且被认为是Galectin-1（GAL-1）和Galectin-3（GAL-3）的潜在靶标。然而，GAL-1和GAL-3的存在和定位以及与瘢痕疙瘩组织中一些结合伴侣的相互作用尚未考虑。在这里，我们表明，在瘢痕疙瘩的皮肤增厚中，Versican，Syndecan-1，纤连蛋白，血压出素-1，TenAscin C，CD44，整联β（1）和N-Cadherin在接近的细长成纤维细胞中被免疫染色。免疫细胞浸润，连接到胶原束，并在微血管内和一些免疫细胞周围。我们还表明，在细胞质中存在GAL-1和GAL-3，沿着一些成纤维细胞的细胞膜和皮肤增厚的免疫细胞。我们建议GAL-1和GAL-3与成纤维细胞和免疫细胞产生的一些ECM分子，抵消了瘢痕疙瘩中的炎症反应。我们还提出通过其结合伴侣的GAL-1和GAL-3可以在成纤维细胞，免疫细胞，内皮细胞和细胞外空间的细胞表面形成超分子结构，这些细胞表面可能影响成纤维细胞形态，粘附，增殖，迁移，生存以及炎症反应。

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