Tenascin-R plays a role in neuroprotection via its distinct domains that coordinate to modulate the microglia function - PubMed (original) (raw)

. 2005 Mar 4;280(9):8316-23.

doi: 10.1074/jbc.M412730200. Epub 2004 Dec 22.

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

Hong Liao et al. J Biol Chem. 2005.

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Abstract

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

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