PKC mediates inhibitory effects of myelin and chondroitin sulfate proteoglycans on axonal regeneration
Successful axon regeneration in the mammalian central nervous system (CNS) is at least partially compromised due to the inhibitors associated with myelin and glial scar. However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide bioche...
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| Veröffentlicht in: | Nature neuroscience 2004-03, Vol.7 (3), p.261-268 |
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| creator | Sivasankaran, Rajeev Pei, Jiong Wang, Kevin C Zhang, Yi Ping Shields, Christopher B Xu, Xiao-Ming He, Zhigang |
| description | Successful axon regeneration in the mammalian central nervous system (CNS) is at least partially compromised due to the inhibitors associated with myelin and glial scar. However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide biochemical and functional evidence that conventional isoforms of protein kinase C (PKC) are key components in the signaling pathways that mediate the inhibitory activities of myelin components and chondroitin sulfate proteoglycans (CSPGs), the major class of inhibitors in the glial scar. Both the myelin inhibitors and CSPGs induce PKC activation. Blocking PKC activity pharmacologically and genetically attenuates the ability of CNS myelin and CSPGs to activate Rho and inhibit neurite outgrowth. Intrathecal infusion of a PKC inhibitor, Gö6976, into the site of dorsal hemisection promotes regeneration of dorsal column axons across and beyond the lesion site in adult rats. Thus, perturbing PKC activity could represent a therapeutic approach to stimulating axon regeneration after brain and spinal cord injuries. |
| doi_str_mv | 10.1038/nn1193 |
| format | Article |
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However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide biochemical and functional evidence that conventional isoforms of protein kinase C (PKC) are key components in the signaling pathways that mediate the inhibitory activities of myelin components and chondroitin sulfate proteoglycans (CSPGs), the major class of inhibitors in the glial scar. Both the myelin inhibitors and CSPGs induce PKC activation. Blocking PKC activity pharmacologically and genetically attenuates the ability of CNS myelin and CSPGs to activate Rho and inhibit neurite outgrowth. Intrathecal infusion of a PKC inhibitor, Gö6976, into the site of dorsal hemisection promotes regeneration of dorsal column axons across and beyond the lesion site in adult rats. Thus, perturbing PKC activity could represent a therapeutic approach to stimulating axon regeneration after brain and spinal cord injuries.</description><identifier>ISSN: 1097-6256</identifier><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/nn1193</identifier><identifier>PMID: 14770187</identifier><identifier>CODEN: NANEFN</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Animal Genetics and Genomics ; Animals ; Axons ; Behavioral Sciences ; Biological Techniques ; Biomedical and Life Sciences ; Biomedicine ; Cells, Cultured ; Central Nervous System - cytology ; Central Nervous System - growth & development ; Central Nervous System - injuries ; Chondroitin ; Chondroitin Sulfate Proteoglycans - metabolism ; Chondroitin Sulfate Proteoglycans - pharmacology ; Enzyme Inhibitors - pharmacology ; Female ; Growth Cones - drug effects ; Growth Cones - metabolism ; Growth Cones - ultrastructure ; Myelin proteins ; Myelin Proteins - metabolism ; Myelin Proteins - pharmacology ; Myelin-Associated Glycoprotein - metabolism ; Myelin-Associated Glycoprotein - pharmacology ; Nerve Regeneration - drug effects ; Nerve Regeneration - physiology ; Neural Pathways - cytology ; Neural Pathways - growth & development ; Neural Pathways - metabolism ; Neurobiology ; Neurosciences ; Nogo Proteins ; Physiological aspects ; Protein Isoforms - antagonists & inhibitors ; Protein Isoforms - genetics ; Protein Isoforms - metabolism ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - genetics ; Protein Kinase C - metabolism ; Protein kinases ; Rats ; Rats, Sprague-Dawley ; Recombinant Fusion Proteins - metabolism ; Recombinant Fusion Proteins - pharmacology ; Recovery of Function - drug effects ; Recovery of Function - physiology ; Repressor Proteins - metabolism ; Repressor Proteins - pharmacology ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Spinal Cord - cytology ; Spinal Cord - growth & development ; Spinal Cord - metabolism ; Treatment Outcome</subject><ispartof>Nature neuroscience, 2004-03, Vol.7 (3), p.261-268</ispartof><rights>Springer Nature America, Inc. 2004</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-ead96f909182118c5d275cb9ba3673ce13a742e8ab7fc9407c85d6afe8dab50a3</citedby><cites>FETCH-LOGICAL-c504t-ead96f909182118c5d275cb9ba3673ce13a742e8ab7fc9407c85d6afe8dab50a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nn1193$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nn1193$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14770187$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sivasankaran, Rajeev</creatorcontrib><creatorcontrib>Pei, Jiong</creatorcontrib><creatorcontrib>Wang, Kevin C</creatorcontrib><creatorcontrib>Zhang, Yi Ping</creatorcontrib><creatorcontrib>Shields, Christopher B</creatorcontrib><creatorcontrib>Xu, Xiao-Ming</creatorcontrib><creatorcontrib>He, Zhigang</creatorcontrib><title>PKC mediates inhibitory effects of myelin and chondroitin sulfate proteoglycans on axonal regeneration</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><addtitle>Nat Neurosci</addtitle><description>Successful axon regeneration in the mammalian central nervous system (CNS) is at least partially compromised due to the inhibitors associated with myelin and glial scar. However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide biochemical and functional evidence that conventional isoforms of protein kinase C (PKC) are key components in the signaling pathways that mediate the inhibitory activities of myelin components and chondroitin sulfate proteoglycans (CSPGs), the major class of inhibitors in the glial scar. Both the myelin inhibitors and CSPGs induce PKC activation. Blocking PKC activity pharmacologically and genetically attenuates the ability of CNS myelin and CSPGs to activate Rho and inhibit neurite outgrowth. Intrathecal infusion of a PKC inhibitor, Gö6976, into the site of dorsal hemisection promotes regeneration of dorsal column axons across and beyond the lesion site in adult rats. 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Academic</collection><jtitle>Nature neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sivasankaran, Rajeev</au><au>Pei, Jiong</au><au>Wang, Kevin C</au><au>Zhang, Yi Ping</au><au>Shields, Christopher B</au><au>Xu, Xiao-Ming</au><au>He, Zhigang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PKC mediates inhibitory effects of myelin and chondroitin sulfate proteoglycans on axonal regeneration</atitle><jtitle>Nature neuroscience</jtitle><stitle>Nat Neurosci</stitle><addtitle>Nat Neurosci</addtitle><date>2004-03-01</date><risdate>2004</risdate><volume>7</volume><issue>3</issue><spage>261</spage><epage>268</epage><pages>261-268</pages><issn>1097-6256</issn><eissn>1546-1726</eissn><coden>NANEFN</coden><abstract>Successful axon regeneration in the mammalian central nervous system (CNS) is at least partially compromised due to the inhibitors associated with myelin and glial scar. However, the intracellular signaling mechanisms underlying these inhibitory activities are largely unknown. Here we provide biochemical and functional evidence that conventional isoforms of protein kinase C (PKC) are key components in the signaling pathways that mediate the inhibitory activities of myelin components and chondroitin sulfate proteoglycans (CSPGs), the major class of inhibitors in the glial scar. Both the myelin inhibitors and CSPGs induce PKC activation. Blocking PKC activity pharmacologically and genetically attenuates the ability of CNS myelin and CSPGs to activate Rho and inhibit neurite outgrowth. Intrathecal infusion of a PKC inhibitor, Gö6976, into the site of dorsal hemisection promotes regeneration of dorsal column axons across and beyond the lesion site in adult rats. Thus, perturbing PKC activity could represent a therapeutic approach to stimulating axon regeneration after brain and spinal cord injuries.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>14770187</pmid><doi>10.1038/nn1193</doi><tpages>8</tpages></addata></record> |
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| subjects | Animal Genetics and Genomics Animals Axons Behavioral Sciences Biological Techniques Biomedical and Life Sciences Biomedicine Cells, Cultured Central Nervous System - cytology Central Nervous System - growth & development Central Nervous System - injuries Chondroitin Chondroitin Sulfate Proteoglycans - metabolism Chondroitin Sulfate Proteoglycans - pharmacology Enzyme Inhibitors - pharmacology Female Growth Cones - drug effects Growth Cones - metabolism Growth Cones - ultrastructure Myelin proteins Myelin Proteins - metabolism Myelin Proteins - pharmacology Myelin-Associated Glycoprotein - metabolism Myelin-Associated Glycoprotein - pharmacology Nerve Regeneration - drug effects Nerve Regeneration - physiology Neural Pathways - cytology Neural Pathways - growth & development Neural Pathways - metabolism Neurobiology Neurosciences Nogo Proteins Physiological aspects Protein Isoforms - antagonists & inhibitors Protein Isoforms - genetics Protein Isoforms - metabolism Protein Kinase C - antagonists & inhibitors Protein Kinase C - genetics Protein Kinase C - metabolism Protein kinases Rats Rats, Sprague-Dawley Recombinant Fusion Proteins - metabolism Recombinant Fusion Proteins - pharmacology Recovery of Function - drug effects Recovery of Function - physiology Repressor Proteins - metabolism Repressor Proteins - pharmacology Signal Transduction - drug effects Signal Transduction - physiology Spinal Cord - cytology Spinal Cord - growth & development Spinal Cord - metabolism Treatment Outcome |
| title | PKC mediates inhibitory effects of myelin and chondroitin sulfate proteoglycans on axonal regeneration |
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