title: Regulatory function of glycosphingolipids in the inflammation and degeneration.
abstract: Recent progress in the biological sciences has revealed that a number of extrinsic and intrinsic environmental factors may cause chronic inflammation. When these insults are persistent or intermittently repeated, regardless of extrinsic or intrinsic origins, homeostasis of our bodies would be disturbed and undergo long-term impact. These situations might give rise to chronic inflammation, leading to various diseases as results of accumulative effects of various inflammatory reactions. Complex carbohydrates expressed mainly on the cell surface have been demonstrated to play roles in fine-tuning of various biological processes to maintain homeostasis of cells, organs and our bodies. When abnormal physicochemical insults and harmful pathogens invade, the fine-tuning including modification of the glycosylation patterns is continuously exerted. Therefore, defects in the proper response with proper glycosylation lead to chronic inflammation and subsequent deterioration of individual tissues and organs. Genetic depletion of sialic acid-containing glycolipids, gangliosides resulted in the inflammation of CNS and neurodegeneration. Lactosylceramide was also reported to mediate neuroinflammation, leading to chronic inflammatory diseases. Defects of globoseries glycolipids resulted in the increased sensitivity to LPS toxicity. Thus, possibilities that manipulation of synthesis and expression of glycosphingolipids may be applicable for the disease control are now proposed.
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan. Electronic address: koichi@med.nagoya-u.ac.jp.
authors: Koichi
authors: K
authors: Furukawa
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan.
authors: Yuhsuke
authors: Y
authors: Ohmi
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan.
authors: Yuji
authors: Y
authors: Kondo
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan.
authors: Yuki
authors: Y
authors: Ohkawa
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan; Department of Life and Medical Sciences, Chubu University Faculty of Life and Health Sciences, Japan.
authors: Orie
authors: O
authors: Tajima
authors: Department of Biochemistry II, Nagoya University Graduate School of Medicine, Japan; Department of Life and Medical Sciences, Chubu University Faculty of Life and Health Sciences, Japan.
authors: Keiko
authors: K
authors: Furukawa
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism / Q000473:pathology; D003167:Complement Activation; D005732:Gangliosides / Q000235:genetics / Q000378:metabolism; D005915:Globosides / Q000378:metabolism; D006028:Glycosphingolipids / Q000235:genetics / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D018345:Mice, Knockout; D009154:Mutation; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000473:pathology; D009457:Neuroglia / Q000502:physiology; D013116:Spinal Cord / Q000378:metabolism / Q000473:pathology
chemical_list: D005732:Gangliosides; D005915:Globosides; D006028:Glycosphingolipids
keywords: Glycosphingolipid; Inflammation; Neurodegeneration