Calcineurin inhibition enhances motor neuron survival following injury
The immunosuppressive agents cyclosporin A (CsA) and FK‐506 have previously been shown to exhibit neurotrophic and neuroprotective properties in vivo. Given that significant clinical expertise exists for both drugs, they represent an attractive starting point for treatment of acute neural injuries....
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2010-03, Vol.14 (3), p.671-686 |
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| creator | Hui, Kelvin K.W. Liadis, Nicole Robertson, Jennifer Kanungo, Anish Henderson, Jeffrey T. |
| description | The immunosuppressive agents cyclosporin A (CsA) and FK‐506 have previously been shown to exhibit neurotrophic and neuroprotective properties in vivo. Given that significant clinical expertise exists for both drugs, they represent an attractive starting point for treatment of acute neural injuries. One putative mechanism for neuroprotection by these drugs relates to inhibition of calcineurin activity. However each drug–immunophilin complex can potentially influence additional signal transduction pathways. Furthermore, several non‐immunosuppressive immunophilin ligands have been described as possessing neuroprotective properties, suggesting that neuroprotection may be separable from calcineurin inhibition. In the present study, we examined the mechanism of this neuroprotection in facial motor neurons following axotomy‐induced injury. Similar to previous studies in rats, CsA and FK‐506 enhanced motor neuron survival in mice following acute injury. To examine the mechanism responsible for neuroprotection by these agents, pharmacologic inhibitors of several potential alternate signalling pathways (17‐(allylamino)‐17‐demethoxygeldanamycin, rapamycin, cypermethrin) were evaluated with respect to neuroprotection. Of these, only cypermethrin, a direct calcineurin inhibitor not previously associated with neuronal survival properties, was observed to significantly enhance motor neuron survival following injury. The results demonstrate for the first time that direct inhibition of calcineurin is neuroprotective in vivo. These data support a model in which calcineurin inhibition promotes neuronal survival, distinct from effects upon neurite outgrowth. |
| doi_str_mv | 10.1111/j.1582-4934.2009.00715.x |
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Given that significant clinical expertise exists for both drugs, they represent an attractive starting point for treatment of acute neural injuries. One putative mechanism for neuroprotection by these drugs relates to inhibition of calcineurin activity. However each drug–immunophilin complex can potentially influence additional signal transduction pathways. Furthermore, several non‐immunosuppressive immunophilin ligands have been described as possessing neuroprotective properties, suggesting that neuroprotection may be separable from calcineurin inhibition. In the present study, we examined the mechanism of this neuroprotection in facial motor neurons following axotomy‐induced injury. Similar to previous studies in rats, CsA and FK‐506 enhanced motor neuron survival in mice following acute injury. To examine the mechanism responsible for neuroprotection by these agents, pharmacologic inhibitors of several potential alternate signalling pathways (17‐(allylamino)‐17‐demethoxygeldanamycin, rapamycin, cypermethrin) were evaluated with respect to neuroprotection. Of these, only cypermethrin, a direct calcineurin inhibitor not previously associated with neuronal survival properties, was observed to significantly enhance motor neuron survival following injury. The results demonstrate for the first time that direct inhibition of calcineurin is neuroprotective in vivo. These data support a model in which calcineurin inhibition promotes neuronal survival, distinct from effects upon neurite outgrowth.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/j.1582-4934.2009.00715.x</identifier><identifier>PMID: 19243469</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Animals, Newborn ; Apoptosis ; Axonogenesis ; Axotomy ; Calcineurin - genetics ; Calcineurin Inhibitors ; Caspase 3 - metabolism ; Cell Survival - drug effects ; Cyclosporin A ; Cyclosporine - pharmacology ; Cypermethrin ; Cytochrome ; Drug therapy ; Drugs ; Enzyme Activation - drug effects ; facial nerve ; Immunohistochemistry ; immunophilin ligands ; Immunosuppressive agents ; Immunosuppressive Agents - pharmacology ; Insecticides - pharmacology ; Laboratories ; Mice ; Mice, Inbred ICR ; Mice, Inbred Strains ; Mice, Knockout ; Microscopy, Fluorescence ; Motor neurons ; Motor Neurons - drug effects ; Motor Neurons - metabolism ; Motor Neurons - pathology ; neuronal survival ; Neurons ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Pharmaceuticals ; Pharmacology ; Phosphatase ; Phosphorylation ; programmed cell death ; Proteins ; Pyrethrins - pharmacology ; Rapamycin ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; Tacrolimus ; Tacrolimus - pharmacology</subject><ispartof>Journal of cellular and molecular medicine, 2010-03, Vol.14 (3), p.671-686</ispartof><rights>2009 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd</rights><rights>Copyright Blackwell Publishing Ltd. Mar 2010</rights><rights>2010. This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2009 The Authors Journal compilation © 2010 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd 2009</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5285-6f4b4e72daeecc923cf3f6c32d83ec20f2c67d29c91aa664b3a1dc05a43a345c3</citedby><cites>FETCH-LOGICAL-c5285-6f4b4e72daeecc923cf3f6c32d83ec20f2c67d29c91aa664b3a1dc05a43a345c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823465/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823465/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1582-4934.2009.00715.x$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19243469$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hui, Kelvin K.W.</creatorcontrib><creatorcontrib>Liadis, Nicole</creatorcontrib><creatorcontrib>Robertson, Jennifer</creatorcontrib><creatorcontrib>Kanungo, Anish</creatorcontrib><creatorcontrib>Henderson, Jeffrey T.</creatorcontrib><title>Calcineurin inhibition enhances motor neuron survival following injury</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>The immunosuppressive agents cyclosporin A (CsA) and FK‐506 have previously been shown to exhibit neurotrophic and neuroprotective properties in vivo. Given that significant clinical expertise exists for both drugs, they represent an attractive starting point for treatment of acute neural injuries. One putative mechanism for neuroprotection by these drugs relates to inhibition of calcineurin activity. However each drug–immunophilin complex can potentially influence additional signal transduction pathways. Furthermore, several non‐immunosuppressive immunophilin ligands have been described as possessing neuroprotective properties, suggesting that neuroprotection may be separable from calcineurin inhibition. In the present study, we examined the mechanism of this neuroprotection in facial motor neurons following axotomy‐induced injury. Similar to previous studies in rats, CsA and FK‐506 enhanced motor neuron survival in mice following acute injury. To examine the mechanism responsible for neuroprotection by these agents, pharmacologic inhibitors of several potential alternate signalling pathways (17‐(allylamino)‐17‐demethoxygeldanamycin, rapamycin, cypermethrin) were evaluated with respect to neuroprotection. Of these, only cypermethrin, a direct calcineurin inhibitor not previously associated with neuronal survival properties, was observed to significantly enhance motor neuron survival following injury. The results demonstrate for the first time that direct inhibition of calcineurin is neuroprotective in vivo. These data support a model in which calcineurin inhibition promotes neuronal survival, distinct from effects upon neurite outgrowth.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis</subject><subject>Axonogenesis</subject><subject>Axotomy</subject><subject>Calcineurin - genetics</subject><subject>Calcineurin Inhibitors</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Survival - drug effects</subject><subject>Cyclosporin A</subject><subject>Cyclosporine - pharmacology</subject><subject>Cypermethrin</subject><subject>Cytochrome</subject><subject>Drug therapy</subject><subject>Drugs</subject><subject>Enzyme Activation - drug effects</subject><subject>facial nerve</subject><subject>Immunohistochemistry</subject><subject>immunophilin ligands</subject><subject>Immunosuppressive agents</subject><subject>Immunosuppressive Agents - pharmacology</subject><subject>Insecticides - pharmacology</subject><subject>Laboratories</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Microscopy, Fluorescence</subject><subject>Motor neurons</subject><subject>Motor Neurons - drug effects</subject><subject>Motor Neurons - metabolism</subject><subject>Motor Neurons - pathology</subject><subject>neuronal survival</subject><subject>Neurons</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Pharmaceuticals</subject><subject>Pharmacology</subject><subject>Phosphatase</subject><subject>Phosphorylation</subject><subject>programmed cell death</subject><subject>Proteins</subject><subject>Pyrethrins - pharmacology</subject><subject>Rapamycin</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Tacrolimus</subject><subject>Tacrolimus - pharmacology</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkctOwzAQRS0EgvL4BRTBusHPxF6AhCrKQ63YwNpyHYc6Su3iNC39exxaFVgg4Y1HM-dezegCkCCYoviuqhQxjvtUEJpiCEUKYY5Y-rEHervB_rZGnPAjcNw0FYQkQ0QcgiMkMCU0Ez0wHKhaW2faYF1i3dRO7MJ6lxg3VU6bJpn5hQ9JB8Ru04alXao6KX1d-5V1b1FTtWF9Cg5KVTfmbPufgNfh3cvgoT96vn8c3I76mmHO-llJJ9TkuFDGaC0w0SUpM01wwYnRGJZYZ3mBhRZIqSyjE6JQoSFTlChCmSYn4GbjO28nM1No4xZB1XIe7EyFtfTKyt8TZ6fyzS8l4TgezKLB5dYg-PfWNAtZ-Ta4uLMkMGciQ4zxSF38RWGUI06hyCPEN5AOvmmCKXdrICi7mGQluwRkl4bsYpJfMcmPKD3_eca3cJtLBK43wMrWZv1vY_k0GI9jRT4BujGi7Q</recordid><startdate>201003</startdate><enddate>201003</enddate><creator>Hui, Kelvin K.W.</creator><creator>Liadis, Nicole</creator><creator>Robertson, Jennifer</creator><creator>Kanungo, Anish</creator><creator>Henderson, Jeffrey T.</creator><general>Blackwell Publishing Ltd</general><general>John Wiley & Sons, Inc</general><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>K9.</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>201003</creationdate><title>Calcineurin inhibition enhances motor neuron survival following injury</title><author>Hui, Kelvin K.W. ; Liadis, Nicole ; Robertson, Jennifer ; Kanungo, Anish ; Henderson, Jeffrey T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5285-6f4b4e72daeecc923cf3f6c32d83ec20f2c67d29c91aa664b3a1dc05a43a345c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis</topic><topic>Axonogenesis</topic><topic>Axotomy</topic><topic>Calcineurin - genetics</topic><topic>Calcineurin Inhibitors</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Survival - drug effects</topic><topic>Cyclosporin A</topic><topic>Cyclosporine - pharmacology</topic><topic>Cypermethrin</topic><topic>Cytochrome</topic><topic>Drug therapy</topic><topic>Drugs</topic><topic>Enzyme Activation - drug effects</topic><topic>facial nerve</topic><topic>Immunohistochemistry</topic><topic>immunophilin ligands</topic><topic>Immunosuppressive agents</topic><topic>Immunosuppressive Agents - pharmacology</topic><topic>Insecticides - pharmacology</topic><topic>Laboratories</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Microscopy, Fluorescence</topic><topic>Motor neurons</topic><topic>Motor Neurons - drug effects</topic><topic>Motor Neurons - metabolism</topic><topic>Motor Neurons - pathology</topic><topic>neuronal survival</topic><topic>Neurons</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - 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Given that significant clinical expertise exists for both drugs, they represent an attractive starting point for treatment of acute neural injuries. One putative mechanism for neuroprotection by these drugs relates to inhibition of calcineurin activity. However each drug–immunophilin complex can potentially influence additional signal transduction pathways. Furthermore, several non‐immunosuppressive immunophilin ligands have been described as possessing neuroprotective properties, suggesting that neuroprotection may be separable from calcineurin inhibition. In the present study, we examined the mechanism of this neuroprotection in facial motor neurons following axotomy‐induced injury. Similar to previous studies in rats, CsA and FK‐506 enhanced motor neuron survival in mice following acute injury. To examine the mechanism responsible for neuroprotection by these agents, pharmacologic inhibitors of several potential alternate signalling pathways (17‐(allylamino)‐17‐demethoxygeldanamycin, rapamycin, cypermethrin) were evaluated with respect to neuroprotection. Of these, only cypermethrin, a direct calcineurin inhibitor not previously associated with neuronal survival properties, was observed to significantly enhance motor neuron survival following injury. The results demonstrate for the first time that direct inhibition of calcineurin is neuroprotective in vivo. These data support a model in which calcineurin inhibition promotes neuronal survival, distinct from effects upon neurite outgrowth.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19243469</pmid><doi>10.1111/j.1582-4934.2009.00715.x</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Newborn Apoptosis Axonogenesis Axotomy Calcineurin - genetics Calcineurin Inhibitors Caspase 3 - metabolism Cell Survival - drug effects Cyclosporin A Cyclosporine - pharmacology Cypermethrin Cytochrome Drug therapy Drugs Enzyme Activation - drug effects facial nerve Immunohistochemistry immunophilin ligands Immunosuppressive agents Immunosuppressive Agents - pharmacology Insecticides - pharmacology Laboratories Mice Mice, Inbred ICR Mice, Inbred Strains Mice, Knockout Microscopy, Fluorescence Motor neurons Motor Neurons - drug effects Motor Neurons - metabolism Motor Neurons - pathology neuronal survival Neurons Neuroprotection Neuroprotective Agents - pharmacology Pharmaceuticals Pharmacology Phosphatase Phosphorylation programmed cell death Proteins Pyrethrins - pharmacology Rapamycin Rodents Signal transduction Signal Transduction - drug effects Tacrolimus Tacrolimus - pharmacology |
| title | Calcineurin inhibition enhances motor neuron survival following injury |
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