Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice
Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that e...
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description | Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. Activation of PKC has been shown to be involved in the disorganization of actin filaments. In this study, we show that Ro‐31‐8220 reverses growth cone collapse by phorbol 12‐myristate 13‐acetate and suggest that one of the effects of activating PKC on retrograde transport is to disrupt the actin filaments. © 2003 Wiley‐Liss, Inc. |
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Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. Activation of PKC has been shown to be involved in the disorganization of actin filaments. In this study, we show that Ro‐31‐8220 reverses growth cone collapse by phorbol 12‐myristate 13‐acetate and suggest that one of the effects of activating PKC on retrograde transport is to disrupt the actin filaments. © 2003 Wiley‐Liss, Inc.</description><identifier>ISSN: 0360-4012</identifier><identifier>EISSN: 1097-4547</identifier><identifier>DOI: 10.1002/jnr.10568</identifier><identifier>PMID: 12671995</identifier><language>eng</language><publisher>New York: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Actin Cytoskeleton - drug effects ; Animals ; Axonal Transport - drug effects ; Axonal Transport - physiology ; Cell Survival - drug effects ; Enzyme Activators - pharmacology ; Enzyme Inhibitors - pharmacology ; Eye - innervation ; Eye - metabolism ; Growth Cones - drug effects ; Indoles - pharmacology ; Male ; Mice ; Mice, Inbred BALB C ; Nerve Growth Factors - drug effects ; Nerve Growth Factors - metabolism ; Neurons, Afferent - drug effects ; Neurons, Afferent - metabolism ; NGF ; NT4 ; p75NTR ; phorbol esters ; Presynaptic Terminals - drug effects ; Protein Kinase C - antagonists & inhibitors ; Protein Kinase C - drug effects ; Protein Kinase C - metabolism ; Receptor, Nerve Growth Factor - metabolism ; Receptor, trkA - metabolism ; Superior Cervical Ganglion - metabolism ; Sympathetic Nervous System - metabolism ; Tetradecanoylphorbol Acetate - pharmacology ; Trigeminal Ganglion - metabolism ; TrkA</subject><ispartof>Journal of neuroscience research, 2003-04, Vol.72 (2), p.203-210</ispartof><rights>Copyright © 2003 Wiley‐Liss, Inc.</rights><rights>Copyright 2003 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3908-95b5e371af27ab8be44613e75b77487bf35790c4e4419292cc3ec5bbc88de5fb3</citedby><cites>FETCH-LOGICAL-c3908-95b5e371af27ab8be44613e75b77487bf35790c4e4419292cc3ec5bbc88de5fb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjnr.10568$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjnr.10568$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27903,27904,45553,45554</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12671995$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ozsarac, Nesrin</creatorcontrib><creatorcontrib>Weible 2nd, Michael</creatorcontrib><creatorcontrib>Reynolds, Anna J.</creatorcontrib><creatorcontrib>Hendry, Ian A.</creatorcontrib><title>Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice</title><title>Journal of neuroscience research</title><addtitle>J. Neurosci. Res</addtitle><description>Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. Activation of PKC has been shown to be involved in the disorganization of actin filaments. In this study, we show that Ro‐31‐8220 reverses growth cone collapse by phorbol 12‐myristate 13‐acetate and suggest that one of the effects of activating PKC on retrograde transport is to disrupt the actin filaments. © 2003 Wiley‐Liss, Inc.</description><subject>Actin Cytoskeleton - drug effects</subject><subject>Animals</subject><subject>Axonal Transport - drug effects</subject><subject>Axonal Transport - physiology</subject><subject>Cell Survival - drug effects</subject><subject>Enzyme Activators - pharmacology</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Eye - innervation</subject><subject>Eye - metabolism</subject><subject>Growth Cones - drug effects</subject><subject>Indoles - pharmacology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Nerve Growth Factors - drug effects</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neurons, Afferent - drug effects</subject><subject>Neurons, Afferent - metabolism</subject><subject>NGF</subject><subject>NT4</subject><subject>p75NTR</subject><subject>phorbol esters</subject><subject>Presynaptic Terminals - drug effects</subject><subject>Protein Kinase C - antagonists & inhibitors</subject><subject>Protein Kinase C - drug effects</subject><subject>Protein Kinase C - metabolism</subject><subject>Receptor, Nerve Growth Factor - metabolism</subject><subject>Receptor, trkA - metabolism</subject><subject>Superior Cervical Ganglion - metabolism</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Trigeminal Ganglion - metabolism</subject><subject>TrkA</subject><issn>0360-4012</issn><issn>1097-4547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtOAyEUhonRaK0ufAEzKxMXY2GAYViaek-jifGyJEDPKNoyFaiXtxdt1ZWrc3Ly_X9OPoR2CD4gGFeDJx_ywutmBfUIlqJknIlV1MO0xiXDpNpAmzE-YYyl5HQdbZCqFiTvPXR7aJN71cl1vujaYha6BM4Xz87rCMWwcP7RGZdiESCF7iHoMRQpaB9nXUhfCQ_znAnd7NH5mPFi6ixsobVWTyJsL2cf3Z4c3wzPytHV6fnwcFRaKnFTSm44UEF0WwltGgOM1YSC4EYI1gjTUi4ktizfiaxkZS0Fy42xTTMG3hraR3uL3vz3yxxiUlMXLUwm2kM3j4o0smKYyQzuL0AbuhgDtGoW3FSHD0Ww-nKoskP17TCzu8vSuZnC-I9cSsvAYAG8uQl8_N-kLi6vfyrLRcLFBO-_CR2eVS2o4Or-8lQdje5OMCZnakg_ARPNi1M</recordid><startdate>20030415</startdate><enddate>20030415</enddate><creator>Ozsarac, Nesrin</creator><creator>Weible 2nd, Michael</creator><creator>Reynolds, Anna J.</creator><creator>Hendry, Ian A.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20030415</creationdate><title>Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice</title><author>Ozsarac, Nesrin ; Weible 2nd, Michael ; Reynolds, Anna J. ; Hendry, Ian A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3908-95b5e371af27ab8be44613e75b77487bf35790c4e4419292cc3ec5bbc88de5fb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Actin Cytoskeleton - drug effects</topic><topic>Animals</topic><topic>Axonal Transport - drug effects</topic><topic>Axonal Transport - physiology</topic><topic>Cell Survival - drug effects</topic><topic>Enzyme Activators - pharmacology</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Eye - innervation</topic><topic>Eye - metabolism</topic><topic>Growth Cones - drug effects</topic><topic>Indoles - pharmacology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Nerve Growth Factors - drug effects</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neurons, Afferent - drug effects</topic><topic>Neurons, Afferent - metabolism</topic><topic>NGF</topic><topic>NT4</topic><topic>p75NTR</topic><topic>phorbol esters</topic><topic>Presynaptic Terminals - drug effects</topic><topic>Protein Kinase C - antagonists & inhibitors</topic><topic>Protein Kinase C - drug effects</topic><topic>Protein Kinase C - metabolism</topic><topic>Receptor, Nerve Growth Factor - metabolism</topic><topic>Receptor, trkA - metabolism</topic><topic>Superior Cervical Ganglion - metabolism</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Trigeminal Ganglion - metabolism</topic><topic>TrkA</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ozsarac, Nesrin</creatorcontrib><creatorcontrib>Weible 2nd, Michael</creatorcontrib><creatorcontrib>Reynolds, Anna J.</creatorcontrib><creatorcontrib>Hendry, Ian A.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of neuroscience research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ozsarac, Nesrin</au><au>Weible 2nd, Michael</au><au>Reynolds, Anna J.</au><au>Hendry, Ian A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice</atitle><jtitle>Journal of neuroscience research</jtitle><addtitle>J. Neurosci. Res</addtitle><date>2003-04-15</date><risdate>2003</risdate><volume>72</volume><issue>2</issue><spage>203</spage><epage>210</epage><pages>203-210</pages><issn>0360-4012</issn><eissn>1097-4547</eissn><abstract>Retrograde axonal transport of neurotrophins from nerve terminal to cell body requires a number of key processes, including internalization of the receptor‐neurotrophin complex into vesicles and formation of multivesicular bodies and their transport along the axon. Previous studies have shown that each of these processes can be regulated by kinases. In this study, we looked at the role of protein kinase C (PKC) in retrograde transport by injecting labeled neurotrophins together with relevant pharmacological agents into the eye and measuring the accumulation of radioactivity in the trigeminal and superior cervical ganglia. Inhibitors of PKC, Ro‐31‐8220 and rottlerin, did not affect the retrograde transport of nerve growth factor (NGF); however, phorbol ester activation of classical and novel PKCs blocked retrograde transport. The effect of phorbol esters was partially reversed by rottlerin and Ro‐31‐8220. Activation of PKC has been shown to be involved in the disorganization of actin filaments. In this study, we show that Ro‐31‐8220 reverses growth cone collapse by phorbol 12‐myristate 13‐acetate and suggest that one of the effects of activating PKC on retrograde transport is to disrupt the actin filaments. © 2003 Wiley‐Liss, Inc.</abstract><cop>New York</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>12671995</pmid><doi>10.1002/jnr.10568</doi><tpages>8</tpages></addata></record> |
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subjects | Actin Cytoskeleton - drug effects Animals Axonal Transport - drug effects Axonal Transport - physiology Cell Survival - drug effects Enzyme Activators - pharmacology Enzyme Inhibitors - pharmacology Eye - innervation Eye - metabolism Growth Cones - drug effects Indoles - pharmacology Male Mice Mice, Inbred BALB C Nerve Growth Factors - drug effects Nerve Growth Factors - metabolism Neurons, Afferent - drug effects Neurons, Afferent - metabolism NGF NT4 p75NTR phorbol esters Presynaptic Terminals - drug effects Protein Kinase C - antagonists & inhibitors Protein Kinase C - drug effects Protein Kinase C - metabolism Receptor, Nerve Growth Factor - metabolism Receptor, trkA - metabolism Superior Cervical Ganglion - metabolism Sympathetic Nervous System - metabolism Tetradecanoylphorbol Acetate - pharmacology Trigeminal Ganglion - metabolism TrkA |
title | Activation of protein kinase C inhibits retrograde transport of neurotrophins in mice |
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