Cellular and Molecular Biology



Emerging role of tissue lectins as microenvironmental effectors in tumors and wounds

Karel Smetana Jr1, Pavol Szabo1, Peter Gál1,2,3, Sabine André4, Hans-Joachim Gabius4, Ondřej Kodet1,5 and Barbora Dvořánková1

1Charles University, 1st Faculty of Medicine, Institute of Anatomy, Prague, Czech Republic, 2East-Slovak Institute of Cardiovascular Diseases, Department for Biomedical Research, Košice, Slovak Republic, 3Pavol Jozef Šafárik University, Faculty of Medicine, Department of Pharmacology, Košice, Slovak Republic, 4Ludwig-Maximilians-University Munich, Faculty of Veterinary Medicine, Institute of Physiological Chemistry, Munich, Germany and 5Charles University, 1st Faculty of Medicine, Department of Dermatovenerology, Prague, Czech Republic

Offprint requests to: Barbora Dvořánková, Charles University, 1st Faculty of Medicine, Institute of Anatomy, U Nemocnice 3, 128 00 Prague 2, Czech Republic. e-mail: bdvorankova@seznam.cz

Summary. Detailed comparative analysis of at first sight not related process cascades is a means toward this aim: to trace common effector mechanisms and hereby eventually inspire innovative routes for therapeutic management. Following this concept, promotion of tumor progression by stroma, especially cancer-associated fibroblasts and smooth muscle actin-positive myofibroblasts, and beneficial activity of respective cells in wound healing have helped to delineate the involvement of endogenous lectins of the family of galectins. In addition to initiating conversion of fibroblasts to myofibroblasts, galectin-1 instructs the cells to produce a structurally complex extracellular matrix. This bioscaffold is useful for keratinocyte culture, also apparently operative in ameliorating wound healing. These functional aspects encourage to study in detail how lectin-(glycan) counterreceptor display is orchestrated. Such insights are assumed to have potential to contribute to rationally manipulate stem/precursor cells as resource in regenerative medicine. Histol Histopathol 30, 293-309 (2015)

Key words: Chemokine, Fibroblast, Glycosylation, Lectin, Myofibroblast, Stem cell

DOI: 10.14670/HH-30.293