Deficient activation of microglia during optic nerve degeneration |
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Authors: | Fanny Reichert Shlomo Rotshenker |
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Affiliation: | Department of Anatomy and Cell Biology, Hebrew University Hadassah Medical School, P.O. Box 12772, Jerusalem 91120, Israel |
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Abstract: | Transection of an optic nerve (ON) is followed by slow removal of myelin. We studied microglia for the expression of molecules that characterize activated myelin phagocytosing macrophages: MAC-1, FcγII/III receptor (FcR), MAC-2, and F4/80. In-vitro, microglia expressed all molecules and phagocytosed myelin. In-vivo, intact ON displayed high levels of MAC-1, little FcR and F4/80, and no MAC-2. The expression of these molecules was upregulated differentially in in-vivo degenerating ON: MAC-1 uniformly, FcR and F4/80 variably, and MAC-2 sporadically. The distribution of MAC-2 expression correlated best with a pattern of sporadic structural degeneration. Thus in-vivo, ON injury is followed by deficient microglia activation, which we suggest contributes significantly to the slow clearance of myelin. |
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Keywords: | nerve transection nerve degeneration demyelination microglia myelin |
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