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.
Department of Anatomy, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan; Japan Science and Technology, Tokyo 142-8555, Japan. yin@med.showa-u.ac.jp
Li
L
Yin
Hirokazu
H
Ohtaki
Tomoya
T
Nakamachi
Yoshifumi
Y
Kudo
Reiko
R
Makino
Seiji
S
Shioda
D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases / Q000378:metabolism; D000818:Animals; D000943:Antigens, Differentiation / Q000378:metabolism; D001253:Astrocytes / Q000378:metabolism*; D005455:Fluorescent Antibody Technique / Q000379:methods; D007839:Functional Laterality / Q000502:physiology; D005786:Gene Expression Regulation / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D016900:Neurofilament Proteins / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D047888:Receptors, Tumor Necrosis Factor, Type I; D015427:Reperfusion Injury / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013997:Time Factors; D053319:Tumor Necrosis Factor Decoy Receptors
D000943:Antigens, Differentiation; D005904:Glial Fibrillary Acidic Protein; D008869:Microtubule-Associated Proteins; C079240:Mtap2 protein, mouse; D016900:Neurofilament Proteins; D012333:RNA, Messenger; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D053319:Tumor Necrosis Factor Decoy Receptors; C036763:monocyte-macrophage differentiation antigen; C051774:neurofilament protein H; D018799:Intercellular Adhesion Molecule-1; C069521:recombinant human tumor necrosis factor-binding protein-1; D015087:2',3'-Cyclic-Nucleotide Phosphodiesterases