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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...

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Autores principales: Sherman, Larry S., Matsumoto, Steven, Su, Weiping, Srivastava, Taasin, Back, Stephen A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2015
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.
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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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