Delayed expressed TNFR1 co-localize with ICAM-1 in astrocyte in mice brain after transient focal ischemia.

Intercellular adhesion molecule-1 (ICAM-1) is expressed after brain ischemia and is participated in the induction of neuronal cell death. Recently, we have reported that ICAM-1 is localized in astrocytes in the chronic phase of ischemia. However, the regulation of astroglial ICAM-1 after brain ischemia is not elucidated in detail. Therefore, we examined the gene and protein expression of TNFR1 after transient middle cerebral artery occlusion (tMCAO) by using real time-PCR and immunohistochemistry. Moreover, we determined the relationship of TNFR1 and ICAM-1 in the astrocyte in chronic phase of ischemia. Increased expression of TNFR1 mRNA in the ipsilateral cortex was noted slightly during ischemia and was significantly increased at 12 h after reperfusion. Few TNFR1-like imuunoreactivity (TNFR1-LI) was observed in the cortex of normal animals. However, TNFR1-LI was increased at 1 h during ischemia, then it was decreased at 3-6 h, and was increased again at 12-24 h after reperfusion in the core of ischemic area. TNFR1-LI was demonstrated in both neurons and astrocytes but not in oligodendrocytes and microglia/macrophages at 24 h after reperfusion. At 96 h after tMCAO, TNFR1-LI was increased in the perifocal region and it appeared to be displayed the astrocyte-like cells. By use of double immunostaining method, we found that the ICAM-1-LI was overlapped with GFAP-LI. Our data indicates that the expression of TNFR1 is up-regulated in accordance with ischemic insult and delayed expressed TNFR1-LI co-localized with ICAM-1-LI in astrocytes after tMCAO. These results suggest that astroglial ICAM-1 is regulated by TNF-alpha dependent pathway.