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Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases
The glycosaminoglycan hyaluronan (HA), a component of the extracellular matrix, has been implicated in regulating neural differentiation, survival, proliferation, migration, and cell signaling in the mammalian central nervous system (CNS). HA is found throughout the CNS as a constituent of proteogly...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581574/ https://www.ncbi.nlm.nih.gov/pubmed/26448752 http://dx.doi.org/10.1155/2015/368584 |
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author | Sherman, Larry S. Matsumoto, Steven Su, Weiping Srivastava, Taasin Back, Stephen A. |
author_facet | Sherman, Larry S. Matsumoto, Steven Su, Weiping Srivastava, Taasin Back, Stephen A. |
author_sort | Sherman, Larry S. |
collection | PubMed |
description | The glycosaminoglycan hyaluronan (HA), a component of the extracellular matrix, has been implicated in regulating neural differentiation, survival, proliferation, migration, and cell signaling in the mammalian central nervous system (CNS). HA is found throughout the CNS as a constituent of proteoglycans, especially within perineuronal nets that have been implicated in regulating neuronal activity. HA is also found in the white matter where it is diffusely distributed around astrocytes and oligodendrocytes. Insults to the CNS lead to long-term elevation of HA within damaged tissues, which is linked at least in part to increased transcription of HA synthases. HA accumulation is often accompanied by elevated expression of at least some transmembrane HA receptors including CD44. Hyaluronidases that digest high molecular weight HA into smaller fragments are also elevated following CNS insults and can generate HA digestion products that have unique biological activities. A number of studies, for example, suggest that both the removal of high molecular weight HA and the accumulation of hyaluronidase-generated HA digestion products can impact CNS injuries through mechanisms that include the regulation of progenitor cell differentiation and proliferation. These studies, reviewed here, suggest that targeting HA synthesis, catabolism, and signaling are all potential strategies to promote CNS repair. |
format | Online Article Text |
id | pubmed-4581574 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-45815742015-10-07 Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases Sherman, Larry S. Matsumoto, Steven Su, Weiping Srivastava, Taasin Back, Stephen A. Int J Cell Biol Review Article The glycosaminoglycan hyaluronan (HA), a component of the extracellular matrix, has been implicated in regulating neural differentiation, survival, proliferation, migration, and cell signaling in the mammalian central nervous system (CNS). HA is found throughout the CNS as a constituent of proteoglycans, especially within perineuronal nets that have been implicated in regulating neuronal activity. HA is also found in the white matter where it is diffusely distributed around astrocytes and oligodendrocytes. Insults to the CNS lead to long-term elevation of HA within damaged tissues, which is linked at least in part to increased transcription of HA synthases. HA accumulation is often accompanied by elevated expression of at least some transmembrane HA receptors including CD44. Hyaluronidases that digest high molecular weight HA into smaller fragments are also elevated following CNS insults and can generate HA digestion products that have unique biological activities. A number of studies, for example, suggest that both the removal of high molecular weight HA and the accumulation of hyaluronidase-generated HA digestion products can impact CNS injuries through mechanisms that include the regulation of progenitor cell differentiation and proliferation. These studies, reviewed here, suggest that targeting HA synthesis, catabolism, and signaling are all potential strategies to promote CNS repair. Hindawi Publishing Corporation 2015 2015-09-10 /pmc/articles/PMC4581574/ /pubmed/26448752 http://dx.doi.org/10.1155/2015/368584 Text en Copyright © 2015 Larry S. Sherman et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Sherman, Larry S. Matsumoto, Steven Su, Weiping Srivastava, Taasin Back, Stephen A. Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title | Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title_full | Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title_fullStr | Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title_full_unstemmed | Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title_short | Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases |
title_sort | hyaluronan synthesis, catabolism, and signaling in neurodegenerative diseases |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581574/ https://www.ncbi.nlm.nih.gov/pubmed/26448752 http://dx.doi.org/10.1155/2015/368584 |
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