The Role of Peripheral Myelin Protein 2 in Remyelination
The protein component of the myelin layer is essential for all aspects of peripheral nerves, and its deficiency can lead to structural and functional impairment. The presence of peripheral myelin protein 2 (P2, PMP2, FABP8, M-FABP) in Schwann cells has been known for decades and shown recently to be...
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| Veröffentlicht in: | Cellular and molecular neurobiology 2018-03, Vol.38 (2), p.487-496 |
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| creator | Stettner, Mark Zenker, Jennifer Klingler, Fabian Szepanowski, Fabian Hartung, Hans-P. Mausberg, Anne K. Kleinschnitz, Christoph Chrast, Roman Kieseier, Bernd C. |
| description | The protein component of the myelin layer is essential for all aspects of peripheral nerves, and its deficiency can lead to structural and functional impairment. The presence of peripheral myelin protein 2 (P2, PMP2, FABP8, M-FABP) in Schwann cells has been known for decades and shown recently to be involved in the lipid homeostasis in the peripheral neural system. However, its precise role during de- and remyelination has yet to be elucidated. To this end, we assessed remyelination after sciatic nerve crush injury in vivo, and in an experimental de/remyelination ex vivo myelinating culture model in P2-deficient
(P2
−/−
)
and wild-type (
WT
) animals. In vivo, the nerve crush paradigm revealed temporal structural and functional changes in
P2
−/−
mice as compared to
WT
animals. Concomitantly,
P2
−/−
DRG cultures demonstrated the presence of shorter internodes and enlarged nodes after ex vivo de/remyelination. Together, these data indicate that P2 may play a role in remyelination of the injured peripheral nervous system, presumably by affecting the nodal and internodal configuration. |
| doi_str_mv | 10.1007/s10571-017-0494-0 |
| format | Article |
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(P2
−/−
)
and wild-type (
WT
) animals. In vivo, the nerve crush paradigm revealed temporal structural and functional changes in
P2
−/−
mice as compared to
WT
animals. Concomitantly,
P2
−/−
DRG cultures demonstrated the presence of shorter internodes and enlarged nodes after ex vivo de/remyelination. Together, these data indicate that P2 may play a role in remyelination of the injured peripheral nervous system, presumably by affecting the nodal and internodal configuration.</description><identifier>ISSN: 0272-4340</identifier><identifier>EISSN: 1573-6830</identifier><identifier>DOI: 10.1007/s10571-017-0494-0</identifier><identifier>PMID: 28447247</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Cell culture ; Coculture Techniques ; Fatty acid-binding protein ; Homeostasis ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myelin ; Myelin P2 Protein - physiology ; Myelination ; Nervous system ; Neural Conduction - physiology ; Neurobiology ; Neurosciences ; Original Research ; Peripheral nerves ; Proteins ; Remyelination - physiology ; Rodents ; Schwann cells ; Schwann Cells - pathology ; Schwann Cells - physiology ; Sciatic nerve ; Sciatic Neuropathy - metabolism ; Sciatic Neuropathy - pathology ; Structure-function relationships</subject><ispartof>Cellular and molecular neurobiology, 2018-03, Vol.38 (2), p.487-496</ispartof><rights>Springer Science+Business Media New York 2017</rights><rights>Copyright Springer Science & Business Media 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-1f361638186a50231d64d1cae767e199fa39af75914cd731751908a81e49adf33</citedby><cites>FETCH-LOGICAL-c410t-1f361638186a50231d64d1cae767e199fa39af75914cd731751908a81e49adf33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10571-017-0494-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10571-017-0494-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28447247$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:137690393$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Stettner, Mark</creatorcontrib><creatorcontrib>Zenker, Jennifer</creatorcontrib><creatorcontrib>Klingler, Fabian</creatorcontrib><creatorcontrib>Szepanowski, Fabian</creatorcontrib><creatorcontrib>Hartung, Hans-P.</creatorcontrib><creatorcontrib>Mausberg, Anne K.</creatorcontrib><creatorcontrib>Kleinschnitz, Christoph</creatorcontrib><creatorcontrib>Chrast, Roman</creatorcontrib><creatorcontrib>Kieseier, Bernd C.</creatorcontrib><title>The Role of Peripheral Myelin Protein 2 in Remyelination</title><title>Cellular and molecular neurobiology</title><addtitle>Cell Mol Neurobiol</addtitle><addtitle>Cell Mol Neurobiol</addtitle><description>The protein component of the myelin layer is essential for all aspects of peripheral nerves, and its deficiency can lead to structural and functional impairment. The presence of peripheral myelin protein 2 (P2, PMP2, FABP8, M-FABP) in Schwann cells has been known for decades and shown recently to be involved in the lipid homeostasis in the peripheral neural system. However, its precise role during de- and remyelination has yet to be elucidated. To this end, we assessed remyelination after sciatic nerve crush injury in vivo, and in an experimental de/remyelination ex vivo myelinating culture model in P2-deficient
(P2
−/−
)
and wild-type (
WT
) animals. In vivo, the nerve crush paradigm revealed temporal structural and functional changes in
P2
−/−
mice as compared to
WT
animals. Concomitantly,
P2
−/−
DRG cultures demonstrated the presence of shorter internodes and enlarged nodes after ex vivo de/remyelination. Together, these data indicate that P2 may play a role in remyelination of the injured peripheral nervous system, presumably by affecting the nodal and internodal configuration.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Coculture Techniques</subject><subject>Fatty acid-binding protein</subject><subject>Homeostasis</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myelin</subject><subject>Myelin P2 Protein - physiology</subject><subject>Myelination</subject><subject>Nervous system</subject><subject>Neural Conduction - physiology</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Original Research</subject><subject>Peripheral nerves</subject><subject>Proteins</subject><subject>Remyelination - physiology</subject><subject>Rodents</subject><subject>Schwann cells</subject><subject>Schwann Cells - pathology</subject><subject>Schwann Cells - physiology</subject><subject>Sciatic nerve</subject><subject>Sciatic Neuropathy - metabolism</subject><subject>Sciatic Neuropathy - pathology</subject><subject>Structure-function relationships</subject><issn>0272-4340</issn><issn>1573-6830</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kcFOGzEQhq2qVRNoH4BLtVIvXAwztndtH6uoBSQqUJSeLWd3FpZu1sHOCvH2OCQEqVIvHmv8zT-e-Rk7QThDAH2eEEqNHFBzUFZx-MCmWGrJKyPhI5uC0IIrqWDCjlJ6AAALUH5mE2GU0kLpKTOLeyrmoacitMUtxW59T9H3xe9n6ruhuI1hQzmKIh9zWr1m_aYLwxf2qfV9oq_7eMz-_Pq5mF3y65uLq9mPa14rhA3HVlZYSYOm8iUIiU2lGqw96UoTWtt6aX2rS4uqbrREXaIF4w2Ssr5ppTxmfKebnmg9Lt06disfn13wndun_uYbOWW1wC1_uuPXMTyOlDZu1aWa-t4PFMbk0Ni8FQnWZPT7P-hDGOOQp3Eir9fIylYqU7ij6hhSitQevoDgtja4nQ0u2-C2NjjINd_2yuNyRc2h4m3vGRD7qfLTcEfxvfX_VV8AeoOPZQ</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Stettner, Mark</creator><creator>Zenker, Jennifer</creator><creator>Klingler, Fabian</creator><creator>Szepanowski, Fabian</creator><creator>Hartung, Hans-P.</creator><creator>Mausberg, Anne K.</creator><creator>Kleinschnitz, Christoph</creator><creator>Chrast, Roman</creator><creator>Kieseier, Bernd C.</creator><general>Springer US</general><general>Springer Nature B.V</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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20180301</creationdate><title>The Role of Peripheral Myelin Protein 2 in Remyelination</title><author>Stettner, Mark ; Zenker, Jennifer ; Klingler, Fabian ; Szepanowski, Fabian ; Hartung, Hans-P. ; Mausberg, Anne K. ; Kleinschnitz, Christoph ; Chrast, Roman ; Kieseier, Bernd C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-1f361638186a50231d64d1cae767e199fa39af75914cd731751908a81e49adf33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Coculture Techniques</topic><topic>Fatty acid-binding protein</topic><topic>Homeostasis</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myelin</topic><topic>Myelin P2 Protein - physiology</topic><topic>Myelination</topic><topic>Nervous system</topic><topic>Neural Conduction - physiology</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Original Research</topic><topic>Peripheral nerves</topic><topic>Proteins</topic><topic>Remyelination - physiology</topic><topic>Rodents</topic><topic>Schwann cells</topic><topic>Schwann Cells - pathology</topic><topic>Schwann Cells - physiology</topic><topic>Sciatic nerve</topic><topic>Sciatic Neuropathy - metabolism</topic><topic>Sciatic Neuropathy - pathology</topic><topic>Structure-function relationships</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stettner, Mark</creatorcontrib><creatorcontrib>Zenker, Jennifer</creatorcontrib><creatorcontrib>Klingler, Fabian</creatorcontrib><creatorcontrib>Szepanowski, Fabian</creatorcontrib><creatorcontrib>Hartung, Hans-P.</creatorcontrib><creatorcontrib>Mausberg, Anne K.</creatorcontrib><creatorcontrib>Kleinschnitz, Christoph</creatorcontrib><creatorcontrib>Chrast, Roman</creatorcontrib><creatorcontrib>Kieseier, Bernd C.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><jtitle>Cellular and molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stettner, Mark</au><au>Zenker, Jennifer</au><au>Klingler, Fabian</au><au>Szepanowski, Fabian</au><au>Hartung, Hans-P.</au><au>Mausberg, Anne K.</au><au>Kleinschnitz, Christoph</au><au>Chrast, Roman</au><au>Kieseier, Bernd C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Role of Peripheral Myelin Protein 2 in Remyelination</atitle><jtitle>Cellular and molecular neurobiology</jtitle><stitle>Cell Mol Neurobiol</stitle><addtitle>Cell Mol Neurobiol</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>38</volume><issue>2</issue><spage>487</spage><epage>496</epage><pages>487-496</pages><issn>0272-4340</issn><eissn>1573-6830</eissn><abstract>The protein component of the myelin layer is essential for all aspects of peripheral nerves, and its deficiency can lead to structural and functional impairment. The presence of peripheral myelin protein 2 (P2, PMP2, FABP8, M-FABP) in Schwann cells has been known for decades and shown recently to be involved in the lipid homeostasis in the peripheral neural system. However, its precise role during de- and remyelination has yet to be elucidated. To this end, we assessed remyelination after sciatic nerve crush injury in vivo, and in an experimental de/remyelination ex vivo myelinating culture model in P2-deficient
(P2
−/−
)
and wild-type (
WT
) animals. In vivo, the nerve crush paradigm revealed temporal structural and functional changes in
P2
−/−
mice as compared to
WT
animals. Concomitantly,
P2
−/−
DRG cultures demonstrated the presence of shorter internodes and enlarged nodes after ex vivo de/remyelination. Together, these data indicate that P2 may play a role in remyelination of the injured peripheral nervous system, presumably by affecting the nodal and internodal configuration.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>28447247</pmid><doi>10.1007/s10571-017-0494-0</doi><tpages>10</tpages></addata></record> |
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| ispartof | Cellular and molecular neurobiology, 2018-03, Vol.38 (2), p.487-496 |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell culture Coculture Techniques Fatty acid-binding protein Homeostasis Mice Mice, Inbred C57BL Mice, Knockout Myelin Myelin P2 Protein - physiology Myelination Nervous system Neural Conduction - physiology Neurobiology Neurosciences Original Research Peripheral nerves Proteins Remyelination - physiology Rodents Schwann cells Schwann Cells - pathology Schwann Cells - physiology Sciatic nerve Sciatic Neuropathy - metabolism Sciatic Neuropathy - pathology Structure-function relationships |
| title | The Role of Peripheral Myelin Protein 2 in Remyelination |
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