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Heparin interaction with a receptor on hyperglycemic dividing cells prevents intracellular hyaluronan synthesis and autophagy responses in models of type 1 diabetes |
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| Institution: | 1. Biomedical Engineering, Cleveland Clinic, Cleveland, OH, United States;2. Department of Medicinal Chemistry and Institute for Structural Biology, Virginia Commonwealth University, Richmond, VA, United States;3. Division of Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan;4. Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada;5. Department of Pathobiochemistry, Faculty of Pharmacy, Meijo University, Nagoya, Japan |
| Abstract: | Previous studies and ongoing research indicate the importance of an interaction between a putative receptor on dividing cells in hyperglycemia and the non-reducing end motifs of heparin stored in mast cell secretory granules and how this interaction prevents activation of hyaluronan synthesis in intracellular compartments and subsequent autophagy. This suggests a new role for endosomal heparanase in exposing this cryptic motif present in the initial large heparin chains on serglycin and in the highly sulfated (NS) domains of heparan sulfate. |
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