Loading…

Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging

Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre+/−, MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory...

Full description

Saved in:
Bibliographic Details
Published in:Glia 2020-01, Vol.68 (1), p.161-177
Main Authors: Jha, Mithilesh Kumar, Lee, Youngjin, Russell, Katelyn A., Yang, Fang, Dastgheyb, Raha M., Deme, Pragney, Ament, Xanthe H., Chen, Weiran, Liu, Ying, Guan, Yun, Polydefkis, Michael J., Hoke, Ahmet, Haughey, Norman J., Rothstein, Jeffrey D., Morrison, Brett M.
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943
cites cdi_FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943
container_end_page 177
container_issue 1
container_start_page 161
container_title Glia
container_volume 68
creator Jha, Mithilesh Kumar
Lee, Youngjin
Russell, Katelyn A.
Yang, Fang
Dastgheyb, Raha M.
Deme, Pragney
Ament, Xanthe H.
Chen, Weiran
Liu, Ying
Guan, Yun
Polydefkis, Michael J.
Hoke, Ahmet
Haughey, Norman J.
Rothstein, Jeffrey D.
Morrison, Brett M.
description Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre+/−, MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory, but not motor, peripheral nerves during maturation and aging. Furthermore, reduced mechanical sensitivity is evident in aged P0‐Cre+/−, MCT1 f/f mice. MCT1 deletion in SCs impairs both their glycolytic and mitochondrial functions, leading to altered lipid metabolism of triacylglycerides, diacylglycerides, and sphingomyelin, decreased expression of myelin‐associated glycoprotein, and increased expression of c‐Jun and p75‐neurotrophin receptor, suggesting a regression of SCs to a less mature developmental state. Taken together, our results define the contribution of SC MCT1 to both SC metabolism and peripheral nerve maturation and aging. Main Points SC MCT1 deficiency causes hypomyelination of sensory, but not motor, axons during aging. Selective ablation of MCT1 within SCs impairs glycolytic and mitochondrial functions. SC‐specific MCT1 deficiency impairs proteins that regulate myelin and lipid metabolism in peripheral nerves
doi_str_mv 10.1002/glia.23710
format article
fullrecord <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7054847</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2281115486</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943</originalsourceid><addsrcrecordid>eNp9kU1rFTEUhoNY7LW68QdIwE0RpuYkmY9shFK0LdzShboOmcyZ25SZ5JrMtM6_N7e3FuvCTQ7hPDy8yUvIO2AnwBj_tBmcOeGiBvaCrICppgAQ1UuyYo2SBUgFh-R1SreMQb7Ur8ihAFmKSqoVSVfBB2tiG34tg5mQTtH4tA1xwkiBOk-_2Zt74z21OAyJ2uCn6Np5wkSnQEfj_ITeeIs09DShTyEu1GO8QzouODhvJhc87ebo_IaaTT7fkIPeDAnfPs4j8uPrl-9nF8X6-vzy7HRd2BIkK0plys5IYRveQas4ip4z1ti2K1tUnaxEL0zXcMFNJyrOuWA1L8sG-6ZTrZLiiHzee7dzO2JnMUc3g95GN5q46GCcfr7x7kZvwp2uWSkbWWfB8aMghp8zpkmPLu3-wXgMc9KcNwCQ2SqjH_5Bb8McfX6e5gKEyqAQmfq4p2wMKUXsn8IA07su9a5L_dBlht__Hf8J_VNeBmAP3LsBl_-o9Pn68nQv_Q2pvawR</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2313981133</pqid></control><display><type>article</type><title>Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging</title><source>Wiley:Jisc Collections:Wiley Read and Publish Open Access 2024-2025 (reading list)</source><creator>Jha, Mithilesh Kumar ; Lee, Youngjin ; Russell, Katelyn A. ; Yang, Fang ; Dastgheyb, Raha M. ; Deme, Pragney ; Ament, Xanthe H. ; Chen, Weiran ; Liu, Ying ; Guan, Yun ; Polydefkis, Michael J. ; Hoke, Ahmet ; Haughey, Norman J. ; Rothstein, Jeffrey D. ; Morrison, Brett M.</creator><creatorcontrib>Jha, Mithilesh Kumar ; Lee, Youngjin ; Russell, Katelyn A. ; Yang, Fang ; Dastgheyb, Raha M. ; Deme, Pragney ; Ament, Xanthe H. ; Chen, Weiran ; Liu, Ying ; Guan, Yun ; Polydefkis, Michael J. ; Hoke, Ahmet ; Haughey, Norman J. ; Rothstein, Jeffrey D. ; Morrison, Brett M.</creatorcontrib><description>Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre+/−, MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory, but not motor, peripheral nerves during maturation and aging. Furthermore, reduced mechanical sensitivity is evident in aged P0‐Cre+/−, MCT1 f/f mice. MCT1 deletion in SCs impairs both their glycolytic and mitochondrial functions, leading to altered lipid metabolism of triacylglycerides, diacylglycerides, and sphingomyelin, decreased expression of myelin‐associated glycoprotein, and increased expression of c‐Jun and p75‐neurotrophin receptor, suggesting a regression of SCs to a less mature developmental state. Taken together, our results define the contribution of SC MCT1 to both SC metabolism and peripheral nerve maturation and aging. Main Points SC MCT1 deficiency causes hypomyelination of sensory, but not motor, axons during aging. Selective ablation of MCT1 within SCs impairs glycolytic and mitochondrial functions. SC‐specific MCT1 deficiency impairs proteins that regulate myelin and lipid metabolism in peripheral nerves</description><identifier>ISSN: 0894-1491</identifier><identifier>EISSN: 1098-1136</identifier><identifier>DOI: 10.1002/glia.23710</identifier><identifier>PMID: 31453649</identifier><language>eng</language><publisher>Hoboken, USA: John Wiley &amp; Sons, Inc</publisher><subject>Aging ; Aging - genetics ; Aging - metabolism ; Animals ; Cells, Cultured ; Clonal deletion ; Female ; Glycolysis ; Glycoproteins ; lactate ; Lipid metabolism ; Lipids ; Maintenance ; Male ; Maturation ; MCT1 ; Metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mitochondria ; monocarboxylate transporter ; Monocarboxylic Acid Transporters - deficiency ; Monocarboxylic Acid Transporters - genetics ; Monocarboxylic Acid Transporters - metabolism ; Myelin ; Myelin P0 protein ; Myelin Sheath - genetics ; Myelin Sheath - metabolism ; Myelination ; Neural Conduction - physiology ; peripheral nerve ; Peripheral nerves ; Schwann cell ; Schwann cells ; Schwann Cells - metabolism ; sensory axons ; Sensory neurons ; Sensory Receptor Cells - metabolism ; Sphingomyelin ; Sural Nerve - metabolism ; Symporters - deficiency ; Symporters - genetics ; Symporters - metabolism ; triacylglycerides ; Triglycerides</subject><ispartof>Glia, 2020-01, Vol.68 (1), p.161-177</ispartof><rights>2019 Wiley Periodicals, Inc.</rights><rights>2020 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943</citedby><cites>FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943</cites><orcidid>0000-0001-5194-4122 ; 0000-0002-9526-0053 ; 0000-0003-2001-8470 ; 0000-0001-5404-3899</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31453649$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jha, Mithilesh Kumar</creatorcontrib><creatorcontrib>Lee, Youngjin</creatorcontrib><creatorcontrib>Russell, Katelyn A.</creatorcontrib><creatorcontrib>Yang, Fang</creatorcontrib><creatorcontrib>Dastgheyb, Raha M.</creatorcontrib><creatorcontrib>Deme, Pragney</creatorcontrib><creatorcontrib>Ament, Xanthe H.</creatorcontrib><creatorcontrib>Chen, Weiran</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Guan, Yun</creatorcontrib><creatorcontrib>Polydefkis, Michael J.</creatorcontrib><creatorcontrib>Hoke, Ahmet</creatorcontrib><creatorcontrib>Haughey, Norman J.</creatorcontrib><creatorcontrib>Rothstein, Jeffrey D.</creatorcontrib><creatorcontrib>Morrison, Brett M.</creatorcontrib><title>Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging</title><title>Glia</title><addtitle>Glia</addtitle><description>Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre+/−, MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory, but not motor, peripheral nerves during maturation and aging. Furthermore, reduced mechanical sensitivity is evident in aged P0‐Cre+/−, MCT1 f/f mice. MCT1 deletion in SCs impairs both their glycolytic and mitochondrial functions, leading to altered lipid metabolism of triacylglycerides, diacylglycerides, and sphingomyelin, decreased expression of myelin‐associated glycoprotein, and increased expression of c‐Jun and p75‐neurotrophin receptor, suggesting a regression of SCs to a less mature developmental state. Taken together, our results define the contribution of SC MCT1 to both SC metabolism and peripheral nerve maturation and aging. Main Points SC MCT1 deficiency causes hypomyelination of sensory, but not motor, axons during aging. Selective ablation of MCT1 within SCs impairs glycolytic and mitochondrial functions. SC‐specific MCT1 deficiency impairs proteins that regulate myelin and lipid metabolism in peripheral nerves</description><subject>Aging</subject><subject>Aging - genetics</subject><subject>Aging - metabolism</subject><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Clonal deletion</subject><subject>Female</subject><subject>Glycolysis</subject><subject>Glycoproteins</subject><subject>lactate</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Maintenance</subject><subject>Male</subject><subject>Maturation</subject><subject>MCT1</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Mitochondria</subject><subject>monocarboxylate transporter</subject><subject>Monocarboxylic Acid Transporters - deficiency</subject><subject>Monocarboxylic Acid Transporters - genetics</subject><subject>Monocarboxylic Acid Transporters - metabolism</subject><subject>Myelin</subject><subject>Myelin P0 protein</subject><subject>Myelin Sheath - genetics</subject><subject>Myelin Sheath - metabolism</subject><subject>Myelination</subject><subject>Neural Conduction - physiology</subject><subject>peripheral nerve</subject><subject>Peripheral nerves</subject><subject>Schwann cell</subject><subject>Schwann cells</subject><subject>Schwann Cells - metabolism</subject><subject>sensory axons</subject><subject>Sensory neurons</subject><subject>Sensory Receptor Cells - metabolism</subject><subject>Sphingomyelin</subject><subject>Sural Nerve - metabolism</subject><subject>Symporters - deficiency</subject><subject>Symporters - genetics</subject><subject>Symporters - metabolism</subject><subject>triacylglycerides</subject><subject>Triglycerides</subject><issn>0894-1491</issn><issn>1098-1136</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kU1rFTEUhoNY7LW68QdIwE0RpuYkmY9shFK0LdzShboOmcyZ25SZ5JrMtM6_N7e3FuvCTQ7hPDy8yUvIO2AnwBj_tBmcOeGiBvaCrICppgAQ1UuyYo2SBUgFh-R1SreMQb7Ur8ihAFmKSqoVSVfBB2tiG34tg5mQTtH4tA1xwkiBOk-_2Zt74z21OAyJ2uCn6Np5wkSnQEfj_ITeeIs09DShTyEu1GO8QzouODhvJhc87ebo_IaaTT7fkIPeDAnfPs4j8uPrl-9nF8X6-vzy7HRd2BIkK0plys5IYRveQas4ip4z1ti2K1tUnaxEL0zXcMFNJyrOuWA1L8sG-6ZTrZLiiHzee7dzO2JnMUc3g95GN5q46GCcfr7x7kZvwp2uWSkbWWfB8aMghp8zpkmPLu3-wXgMc9KcNwCQ2SqjH_5Bb8McfX6e5gKEyqAQmfq4p2wMKUXsn8IA07su9a5L_dBlht__Hf8J_VNeBmAP3LsBl_-o9Pn68nQv_Q2pvawR</recordid><startdate>202001</startdate><enddate>202001</enddate><creator>Jha, Mithilesh Kumar</creator><creator>Lee, Youngjin</creator><creator>Russell, Katelyn A.</creator><creator>Yang, Fang</creator><creator>Dastgheyb, Raha M.</creator><creator>Deme, Pragney</creator><creator>Ament, Xanthe H.</creator><creator>Chen, Weiran</creator><creator>Liu, Ying</creator><creator>Guan, Yun</creator><creator>Polydefkis, Michael J.</creator><creator>Hoke, Ahmet</creator><creator>Haughey, Norman J.</creator><creator>Rothstein, Jeffrey D.</creator><creator>Morrison, Brett M.</creator><general>John Wiley &amp; Sons, Inc</general><general>Wiley Subscription Services, 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>7QL</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5194-4122</orcidid><orcidid>https://orcid.org/0000-0002-9526-0053</orcidid><orcidid>https://orcid.org/0000-0003-2001-8470</orcidid><orcidid>https://orcid.org/0000-0001-5404-3899</orcidid></search><sort><creationdate>202001</creationdate><title>Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging</title><author>Jha, Mithilesh Kumar ; Lee, Youngjin ; Russell, Katelyn A. ; Yang, Fang ; Dastgheyb, Raha M. ; Deme, Pragney ; Ament, Xanthe H. ; Chen, Weiran ; Liu, Ying ; Guan, Yun ; Polydefkis, Michael J. ; Hoke, Ahmet ; Haughey, Norman J. ; Rothstein, Jeffrey D. ; Morrison, Brett M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aging</topic><topic>Aging - genetics</topic><topic>Aging - metabolism</topic><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Clonal deletion</topic><topic>Female</topic><topic>Glycolysis</topic><topic>Glycoproteins</topic><topic>lactate</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Maintenance</topic><topic>Male</topic><topic>Maturation</topic><topic>MCT1</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Mitochondria</topic><topic>monocarboxylate transporter</topic><topic>Monocarboxylic Acid Transporters - deficiency</topic><topic>Monocarboxylic Acid Transporters - genetics</topic><topic>Monocarboxylic Acid Transporters - metabolism</topic><topic>Myelin</topic><topic>Myelin P0 protein</topic><topic>Myelin Sheath - genetics</topic><topic>Myelin Sheath - metabolism</topic><topic>Myelination</topic><topic>Neural Conduction - physiology</topic><topic>peripheral nerve</topic><topic>Peripheral nerves</topic><topic>Schwann cell</topic><topic>Schwann cells</topic><topic>Schwann Cells - metabolism</topic><topic>sensory axons</topic><topic>Sensory neurons</topic><topic>Sensory Receptor Cells - metabolism</topic><topic>Sphingomyelin</topic><topic>Sural Nerve - metabolism</topic><topic>Symporters - deficiency</topic><topic>Symporters - genetics</topic><topic>Symporters - metabolism</topic><topic>triacylglycerides</topic><topic>Triglycerides</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jha, Mithilesh Kumar</creatorcontrib><creatorcontrib>Lee, Youngjin</creatorcontrib><creatorcontrib>Russell, Katelyn A.</creatorcontrib><creatorcontrib>Yang, Fang</creatorcontrib><creatorcontrib>Dastgheyb, Raha M.</creatorcontrib><creatorcontrib>Deme, Pragney</creatorcontrib><creatorcontrib>Ament, Xanthe H.</creatorcontrib><creatorcontrib>Chen, Weiran</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Guan, Yun</creatorcontrib><creatorcontrib>Polydefkis, Michael J.</creatorcontrib><creatorcontrib>Hoke, Ahmet</creatorcontrib><creatorcontrib>Haughey, Norman J.</creatorcontrib><creatorcontrib>Rothstein, Jeffrey D.</creatorcontrib><creatorcontrib>Morrison, Brett M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Glia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jha, Mithilesh Kumar</au><au>Lee, Youngjin</au><au>Russell, Katelyn A.</au><au>Yang, Fang</au><au>Dastgheyb, Raha M.</au><au>Deme, Pragney</au><au>Ament, Xanthe H.</au><au>Chen, Weiran</au><au>Liu, Ying</au><au>Guan, Yun</au><au>Polydefkis, Michael J.</au><au>Hoke, Ahmet</au><au>Haughey, Norman J.</au><au>Rothstein, Jeffrey D.</au><au>Morrison, Brett M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging</atitle><jtitle>Glia</jtitle><addtitle>Glia</addtitle><date>2020-01</date><risdate>2020</risdate><volume>68</volume><issue>1</issue><spage>161</spage><epage>177</epage><pages>161-177</pages><issn>0894-1491</issn><eissn>1098-1136</eissn><abstract>Schwann cell (SC)‐specific monocarboxylate transporter 1 (MCT1) knockout mice were generated by mating MCT1 f/f mice with myelin protein zero (P0)‐Cre mice. P0‐Cre+/−, MCT1 f/f mice have no detectable early developmental defects, but develop hypomyelination and reduced conduction velocity in sensory, but not motor, peripheral nerves during maturation and aging. Furthermore, reduced mechanical sensitivity is evident in aged P0‐Cre+/−, MCT1 f/f mice. MCT1 deletion in SCs impairs both their glycolytic and mitochondrial functions, leading to altered lipid metabolism of triacylglycerides, diacylglycerides, and sphingomyelin, decreased expression of myelin‐associated glycoprotein, and increased expression of c‐Jun and p75‐neurotrophin receptor, suggesting a regression of SCs to a less mature developmental state. Taken together, our results define the contribution of SC MCT1 to both SC metabolism and peripheral nerve maturation and aging. Main Points SC MCT1 deficiency causes hypomyelination of sensory, but not motor, axons during aging. Selective ablation of MCT1 within SCs impairs glycolytic and mitochondrial functions. SC‐specific MCT1 deficiency impairs proteins that regulate myelin and lipid metabolism in peripheral nerves</abstract><cop>Hoboken, USA</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>31453649</pmid><doi>10.1002/glia.23710</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0001-5194-4122</orcidid><orcidid>https://orcid.org/0000-0002-9526-0053</orcidid><orcidid>https://orcid.org/0000-0003-2001-8470</orcidid><orcidid>https://orcid.org/0000-0001-5404-3899</orcidid><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0894-1491
ispartof Glia, 2020-01, Vol.68 (1), p.161-177
issn 0894-1491
1098-1136
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7054847
source Wiley:Jisc Collections:Wiley Read and Publish Open Access 2024-2025 (reading list)
subjects Aging
Aging - genetics
Aging - metabolism
Animals
Cells, Cultured
Clonal deletion
Female
Glycolysis
Glycoproteins
lactate
Lipid metabolism
Lipids
Maintenance
Male
Maturation
MCT1
Metabolism
Mice
Mice, Knockout
Mice, Transgenic
Mitochondria
monocarboxylate transporter
Monocarboxylic Acid Transporters - deficiency
Monocarboxylic Acid Transporters - genetics
Monocarboxylic Acid Transporters - metabolism
Myelin
Myelin P0 protein
Myelin Sheath - genetics
Myelin Sheath - metabolism
Myelination
Neural Conduction - physiology
peripheral nerve
Peripheral nerves
Schwann cell
Schwann cells
Schwann Cells - metabolism
sensory axons
Sensory neurons
Sensory Receptor Cells - metabolism
Sphingomyelin
Sural Nerve - metabolism
Symporters - deficiency
Symporters - genetics
Symporters - metabolism
triacylglycerides
Triglycerides
title Monocarboxylate transporter 1 in Schwann cells contributes to maintenance of sensory nerve myelination during aging
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T02%3A38%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Monocarboxylate%20transporter%201%20in%20Schwann%20cells%20contributes%20to%20maintenance%20of%20sensory%20nerve%20myelination%20during%20aging&rft.jtitle=Glia&rft.au=Jha,%20Mithilesh%20Kumar&rft.date=2020-01&rft.volume=68&rft.issue=1&rft.spage=161&rft.epage=177&rft.pages=161-177&rft.issn=0894-1491&rft.eissn=1098-1136&rft_id=info:doi/10.1002/glia.23710&rft_dat=%3Cproquest_pubme%3E2281115486%3C/proquest_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c5140-59a5da43c82d1b92e3f2008cbd5be9d463f3ad8232ad362223072558ef8d9b943%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2313981133&rft_id=info:pmid/31453649&rfr_iscdi=true