Although tenascin-C (TN) is highly up-regulated during the proliferation of reactive astrocytes, little is known about the function of TN at injury sites in the central nervous system (CNS). Here, the function of TN-expressing astrocytes in the injured brain was investigated by analyzing TN-deficient mice with stab-wound injuries of the cerebral cortex. Glial fibrillary acid protein expression after injury was down-regulated earlier in TN-deficient mice than in wild-type (WT) mice. To evaluate immune responses in the injured CNS in the absence of TN, inflammatory cytokine production was examined after unilateral stab injuries of the cerebral cortex in TN-deficient and WT mice. The expression of interleukin (IL)-1β, tumor necrosis factor-α and IL-6 was higher in TN-deficient mice, whereas levels of IL-4 and granulocyte colony-stimulating factor were lower in TN-deficient mice than WT mice. Our findings suggest that TN helps to regulate production of inflammatory cytokines in the injured brain.
|Number of pages||6|
|Publication status||Published - 2008 Jul|
- Central nervous system (CNS)
- Glial fibrillary acidic protein (GFAP)
- Tenascin-C (TN)
ASJC Scopus subject areas