The non-phagocytic route of collagen uptake: a distinct degradation pathway.

摘要: The degradation of collagens, the most abundant proteins extracellular matrix, is involved in numerous physiological and pathological conditions including cancer invasion. An important turnover pathway involves cellular internalization large, soluble collagen fragments, generated by initial cleavage insoluble fibers. We have previously observed that primary mouse fibroblasts, this endocytosis fragments dependent on receptor urokinase plasminogen activator receptor-associated protein (uPARAP)/Endo180. Others identified additional mechanisms uptake, with different associated receptors, other cell types. These receptors include β1-integrins, being responsible for phagocytosis, mannose receptor. now utilized a newly developed monoclonal antibody against uPARAP/Endo180, which down-regulates level treated cells, to examine role uPARAP/Endo180 as mediator wide range cultured With exception macrophages, all cells proved capable efficient were mesenchymal origin these their uptake process. Macrophages internalized process mediated receptor, belonging same family uPARAP/Endo180. β1-Integrins found not be collagen, irrespectively whether was or This further distinguishes pathways from phagocytic particulate collagen.