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Galectin-1 and Galectin-3 and Their Potential Binding Partners in the Dermal Thickening of Keloid Tissues

Arciniegas, Enrique, PhD*; Carrillo, Luz Marina, MSc; Rojas, Héctor, BSc; Ramírez, Richard, BA; Chopite, Marina, MD

The American Journal of Dermatopathology: March 2019 - Volume 41 - Issue 3 - p 193–204
doi: 10.1097/DAD.0000000000001284
Original Study

Abstract: Keloids are defined histopathologically as an inflammatory disorder characterized by exhibiting numerous fibroblasts, abnormal vascularization, increased number of proinflammatory 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 β1, 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.

*Institute of Biomedicine, Central University of Venezuela, Caracas, Venezuela;

Autonomous Service Institute of Biomedicine, Caracas, Venezuela; and

Institute of Immunology, Central University of Venezuela, Caracas, Venezuela.

Correspondence: Enrique Arciniegas, PhD, Instituto de Biomedicina, Universidad Central de Venezuela, Distrito Capital, Caracas 1010, Venezuela (e-mail:

Supported by the Servicio Autónomo Instituto de Biomedicina (SAIB).

The authors declare no conflicts of interest.

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