title: Upregulation of galectin-3 in immortalized Schwann cells IFRS1 under diabetic conditions.
abstract: A spontaneously immortalized adult Fischer rat Schwann cell line IFRS1 retains the characteristic features of normal Schwann cells, and can be a useful tool for the study of diabetic neuropathy. In the present study, we examined the effects of high glucose and 3-deoxyglucosone (3-DG) on the viability and the protein expression of advanced glycation endproducts (AGE)-binding proteins, such as galectin-3 (GAL-3) and receptor for AGE (RAGE) in IFRS1 cells. Exposure to 30mM of glucose or 0.2mM of 3-DG for 7 days failed to impair the IFRS1 cell viability, but significantly upregulated the expression of GAL-3. The same exposure tended to increase the expression of RAGE, but the changes were not significant. The high glucose-induced upregulation of GAL-3 was attenuated by cotreatment with 0.2mM of an anti-glycated agent aminoguanidine or 20nM of an anti-oxidant trans-resveratrol. In addition, treatment of IFRS1 cells with 1μg/ml of recombinant GAL-3 for 48h resulted in the upregulation of B-cell lymphoma 2 (Bcl-2) and the downregulation of 4-hydroxynonenal (4HNE). These findings suggest the involvement of GAL-3 in the glycation and oxidative stress under diabetic conditions and its cytoprotective role in Schwann cells.
authors.affiliation: Laboratory of Peripheral Nerve Pathophysiology, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan; Division of Diabetes, Metabolism & Endocrinology, Department of Internal Medicine, Jikei University School of Medicine, Minato-ku, Tokyo 105-8461, Japan.
authors.forename: Masami
authors.initials: M
authors.lastname: Tsukamoto
authors.affiliation: Laboratory of Peripheral Nerve Pathophysiology, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan. Electronic address: sango-kz@igakuken.or.jp.
authors.forename: Kazunori
authors.initials: K
authors.lastname: Sango
authors.affiliation: Laboratory of Peripheral Nerve Pathophysiology, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
authors.forename: Naoko
authors.initials: N
authors.lastname: Niimi
authors.affiliation: ALS/Neuropathy Project, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
authors.forename: Hiroko
authors.initials: H
authors.lastname: Yanagisawa
authors.affiliation: ALS/Neuropathy Project, Department of Sensory and Motor Systems, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo 156-8506, Japan.
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Watabe
authors.affiliation: Division of Diabetes, Metabolism & Endocrinology, Department of Internal Medicine, Jikei University School of Medicine, Minato-ku, Tokyo 105-8461, Japan.
authors.forename: Kazunori
authors.initials: K
authors.lastname: Utsunomiya
mesh_terms: D000818:Animals; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D003929:Diabetic Neuropathies / Q000378:metabolism*; D037502:Galectin 3 / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology*; D017127:Glycation End Products, Advanced / Q000187:drug effects* / Q000378:metabolism*; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D011916:Rats, Inbred F344; D012583:Schwann Cells / Q000187:drug effects* / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D037502:Galectin 3; D017127:Glycation End Products, Advanced; D005947:Glucose
keywords: Diabetic neuropathy; Galectin-3; Glycation; In vitro; Oxidative stress; Schwann cells