The Responses of Hyperglycemic Dividing Mesangial Cells to Heparin Are Mediated by the Non-reducing Terminal Trisaccharide
© 2015 by The American Society for Biochemistry and Molecular Biology, Inc..
Our previous studies showed: (i) that growth-arrested G0/G1 rat mesangial cells stimulated to divide in hyperglycemic medium initiate intracellular hyaluronan synthesis that induces autophagy and the cyclin D3-induced formation of a monocyte-adhesive extracellular hyaluronan matrix after completing cell division; and (ii) that heparin inhibits the intracellular hyaluronan and autophagy responses, but after completing division, induces hyaluronan synthesis at the plasma membrane with the formation of a larger monocyte-adhesive hyaluronan matrix. This study shows: (i) that the non-terminal trisaccharide of heparin is sufficient to initiate the same responses as intact heparin, (ii) that a fully sulfated tetrasaccharide isolated from bacterial heparin lyase 1 digests of heparin that contains a Δ-2S-iduronate on the non-reducing end does not initiate the same responses as intact heparin, and (iii) that removal of the Δ-2S-iduronate to expose the fully sulfated trisaccharide (GlcNS(6S)-IdoUA(2S)-GlcNS(6S)) does initiate the same responses as intact heparin. These results provide evidence that mammalian heparanase digestion of heparin and heparan sulfate exposes a cryptic motif on the non-reducing termini that is recognized by a receptor on dividing cells.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2015 |
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Erschienen: |
2015 |
Enthalten in: |
Zur Gesamtaufnahme - volume:290 |
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Enthalten in: |
The Journal of biological chemistry - 290(2015), 48 vom: 27. Nov., Seite 29045-50 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Wang, Christina P [VerfasserIn] |
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Links: |
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Anmerkungen: |
Date Completed 18.03.2016 Date Revised 05.02.2021 published: Print-Electronic Citation Status MEDLINE |
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doi: |
10.1074/jbc.M115.677401 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM252832604 |
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520 | |a Our previous studies showed: (i) that growth-arrested G0/G1 rat mesangial cells stimulated to divide in hyperglycemic medium initiate intracellular hyaluronan synthesis that induces autophagy and the cyclin D3-induced formation of a monocyte-adhesive extracellular hyaluronan matrix after completing cell division; and (ii) that heparin inhibits the intracellular hyaluronan and autophagy responses, but after completing division, induces hyaluronan synthesis at the plasma membrane with the formation of a larger monocyte-adhesive hyaluronan matrix. This study shows: (i) that the non-terminal trisaccharide of heparin is sufficient to initiate the same responses as intact heparin, (ii) that a fully sulfated tetrasaccharide isolated from bacterial heparin lyase 1 digests of heparin that contains a Δ-2S-iduronate on the non-reducing end does not initiate the same responses as intact heparin, and (iii) that removal of the Δ-2S-iduronate to expose the fully sulfated trisaccharide (GlcNS(6S)-IdoUA(2S)-GlcNS(6S)) does initiate the same responses as intact heparin. These results provide evidence that mammalian heparanase digestion of heparin and heparan sulfate exposes a cryptic motif on the non-reducing termini that is recognized by a receptor on dividing cells | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, N.I.H., Extramural | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a diabetes | |
650 | 4 | |a diabetic nephropathy | |
650 | 4 | |a endoplasmic reticulum stress (ER stress) | |
650 | 4 | |a glucose metabolism | |
650 | 4 | |a heparanase | |
650 | 4 | |a heparin | |
650 | 4 | |a hyaluronan | |
650 | 4 | |a inflammation | |
650 | 4 | |a monocyte adhesive hyaluronan matrix | |
650 | 4 | |a trisaccharide | |
650 | 7 | |a Trisaccharides |2 NLM | |
650 | 7 | |a Heparin |2 NLM | |
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700 | 1 | |a Hascall, Vincent C |e verfasserin |4 aut | |
700 | 1 | |a Zhang, Fuming |e verfasserin |4 aut | |
700 | 1 | |a Linhardt, Robert J |e verfasserin |4 aut | |
700 | 1 | |a Abbadi, Amina |e verfasserin |4 aut | |
700 | 1 | |a Wang, Aimin |e verfasserin |4 aut | |
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