Tenascin-R plays a role in neuroprotection via its distinct domains that coordinate to modulate the microglia function.

摘要: Microglia are one of the main cell types activated by brain injury. In present study, we have investigated how domains extracellular matrix molecule tenascin-R (TN-R) modulate microglia function. We found that epidermal growth factor-like repeats inhibited adhesion and migration via a protein kinase A-dependent mechanism. contrast, fibronectin 6–8 promoted primary C-dependent Both TN-R induced an up-regulation in secretion cytokines, such as chemokine-induced cytokine 3 tumor neurosis factor α. Interestingly, dramatic brain-derived neurotrophic factor/transforming factor-β nerve factor-β, respectively, conditioned medium from was able to promote neurite outgrowth N1E-115 cells cortical neurons. These results suggest plays role neuroprotection through distinct coordinating