| First Author | Benhamron S | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 5 | Pages | e35602 |
| PubMed ID | 22590508 | Mgi Jnum | J:187248 |
| Mgi Id | MGI:5435978 | Doi | 10.1371/journal.pone.0035602 |
| Citation | Benhamron S, et al. (2012) Dissociation between mature phenotype and impaired transmigration in dendritic cells from heparanase-deficient mice. PLoS One 7(5):e35602 |
| abstractText | To reach the lymphatics, migrating dendritic cells (DCs) need to interact with the extracellular matrix (ECM). Heparanase, a mammalian endo-beta-D-glucuronidase, specifically degrades heparan sulfate proteoglycans ubiquitously associated with the cell surface and ECM. The role of heparanase in the physiology of bone marrow-derived DCs was studied in mutant heparanase knock-out (Hpse-KO) mice. Immature DCs from Hpse-KO mice exhibited a more mature phenotype; however their transmigration was significantly delayed, but not completely abolished, most probably due to the observed upregulation of MMP-14 and CCR7. Despite their mature phenotype, uptake of beads was comparable and uptake of apoptotic cells was more efficient in DCs from Hpse-KO mice. Heparanase is an important enzyme for DC transmigration. Together with CCR7 and its ligands, and probably MMP-14, heparanase controls DC trafficking. |
