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...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2015-01-01
|
| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2015/368584 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832563694174732288 |
|---|---|
| author | Larry S. Sherman Steven Matsumoto Weiping Su Taasin Srivastava Stephen A. Back |
| author_facet | Larry S. Sherman Steven Matsumoto Weiping Su Taasin Srivastava Stephen A. Back |
| author_sort | Larry S. Sherman |
| collection | DOAJ |
| 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 | Article |
| id | doaj-art-32a86055e86a463bb384995a8ede9480 |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-32a86055e86a463bb384995a8ede94802025-02-03T01:12:40ZengWileyInternational Journal of Cell Biology1687-88761687-88842015-01-01201510.1155/2015/368584368584Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative DiseasesLarry S. Sherman0Steven Matsumoto1Weiping Su2Taasin Srivastava3Stephen A. Back4Division of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USADepartment of Integrative Biosciences, School of Dentistry, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USADivision of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USADepartment of Pediatrics, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USADepartment of Pediatrics, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, OR 97239, USAThe 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.http://dx.doi.org/10.1155/2015/368584 |
| spellingShingle | Larry S. Sherman Steven Matsumoto Weiping Su Taasin Srivastava Stephen A. Back Hyaluronan Synthesis, Catabolism, and Signaling in Neurodegenerative Diseases International Journal of Cell Biology |
| 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 |
| url | http://dx.doi.org/10.1155/2015/368584 |
| work_keys_str_mv | AT larryssherman hyaluronansynthesiscatabolismandsignalinginneurodegenerativediseases AT stevenmatsumoto hyaluronansynthesiscatabolismandsignalinginneurodegenerativediseases AT weipingsu hyaluronansynthesiscatabolismandsignalinginneurodegenerativediseases AT taasinsrivastava hyaluronansynthesiscatabolismandsignalinginneurodegenerativediseases AT stephenaback hyaluronansynthesiscatabolismandsignalinginneurodegenerativediseases |