부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brainres.2006.12.036 Byline: Britto P. Nathan (a), Sreenivas Nannapaneni (a), Salina Gairhe (a), Ikemefuna Nwosu (a), Robert G. Struble (b) Keywords: ApoE; Olfactory; Glia; Glial protein; Knockout mice Abbreviations: apoE, apolipoprotein E; OB, olfactory bulb; OE, olfactory epithelium; ORN, olfactory receptor neuron; GBC, globose basal cells; Sus, Sustentacular cells 1 Abstract: Previous studies from our laboratory suggest that apolipoprotein (apoE), a lipid transporting protein, facilitates olfactory nerve regeneration. We have shown that apoE is enriched in the olfactory nerve and around the glomeruli of the olfactory bulb (OB). The studies reported herein were undertaken to identify possible sources of apoE in the olfactory epithelium (OE). Immunoblotting results revealed apoE expression in the OE of wild-type (WT) mice, but not in apoE deficient/knockout (KO) mice. Immunohistochemical studies revealed that the perikarya and processes of sustentacular (Sus) cells expressed apoE-like immunoreactivity. Minimal neuronal apoE immunostaining was seen, although apoE was observed in the interstial spaces between olfactory receptor neurons (ORN). Substantial apoE-like immunoreactivity was localized to the endfeet and terminal process of Sus cells surrounding the basal cells. Double labeling immunocytochemical studies confirmed that the cell bodies and endfeet of Sus cells expressed high levels of apoE. The endothelial cells of blood vessels were intensely stained for apoE in the lamina propria. Cells forming Bowman's gland also immunostained for apoE. The apoE staining in the nerve fascicles was less intense, but was uniformly distributed throughout the core of the nerve bundles. Heavily stained cells, probably ensheathing glia, surrounded the nerve fascicles. These results revealed that apoE is expressed in the adult OE and lamina propria at strategic locations where it could facilitate the differentiation, maturation and axonal growth of the ORN, perhaps by recycling lipids from degenerating ORN for use by growing axons. Author Affiliation: (a) Department of Biological Sciences, Eastern Illinois University, 600 Lincoln Avenue, Charleston, IL 61920, USA (b) Center for Alzheimer's Disease and Related Disorders, PO Box 19628, Southern Illinois School of Medicine, Springfield, IL 62794-9628, USA Article History: Accepted 13 December 2006