title: The expression of syntaphilin is down-regulated in the optic nerve after axonal injury.
abstract: The impairment of mitochondrial function is an important pathogenic factor in glaucoma and other optic neuropathies in which retinal ganglion cell (RGC) death is the fundamental pathology. Syntaphilin was recently discovered as a docking protein that affects mitochondrial mobility. However, no reports have investigated the involvement of syntaphilin in the visual system. We investigated the expression of syntaphilin in the rat retina, optic nerve and brain. The expression of syntaphilin exhibited varying patterns in the visual system. Syntaphilin was expressed in retinal ganglion cells in the retina, in the cell bodies of neurons in the superior colliculus and was abundant in the astrocytes of rat optic nerves (similar to the findings that syntaphilin is expressed in human optic nerves). After optic nerve transection, which caused RGC death and axonal degeneration, quantitative real-time RT-PCR was used to assess changes in gene expression in the rat retina and optic nerve. Syntaphilin gene and protein expression in the optic nerve was downregulated 3 and 7 days after optic nerve transection. Our study suggests that syntaphilin expression in astrocytes at the optic nerve might be involved in axonal injury.
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Akiko
authors.initials: A
authors.lastname: Miki
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan. Electronic address: kanaaki@med.kobe-u.ac.jp.
authors.forename: Akiyasu
authors.initials: A
authors.lastname: Kanamori
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Makoto
authors.initials: M
authors.lastname: Nakamura
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Matsumoto
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Junji
authors.initials: J
authors.lastname: Mizokami
authors.affiliation: Division of Ophthalmology, Department of Surgery, Kobe University Graduate School of Medicine, Kobe, Japan.
authors.forename: Akira
authors.initials: A
authors.lastname: Negi
mesh_terms: D000818:Animals; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics*; D004195:Disease Models, Animal; D015536:Down-Regulation; D007150:Immunohistochemistry; D051379:Mice; D009419:Nerve Tissue Proteins / Q000096:biosynthesis / Q000235:genetics*; D009900:Optic Nerve / Q000378:metabolism* / Q000473:pathology; D020221:Optic Nerve Injuries / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000235:genetics*; D051381:Rats
chemical_list: D002352:Carrier Proteins; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; C000592961:Snph protein, rat
keywords: Axonal injury; Axonal transport; Optic nerve; Syntaphilin; Visual pathway