Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun

After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes...
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Autor*in:	Laura J Wagstaff [verfasserIn] Jose A Gomez-Sanchez [verfasserIn] Shaline V Fazal [verfasserIn] Georg W Otto [verfasserIn] Alastair M Kilpatrick [verfasserIn] Kirolos Michael [verfasserIn] Liam YN Wong [verfasserIn] Ki H Ma [verfasserIn] Mark Turmaine [verfasserIn] John Svaren [verfasserIn] Tessa Gordon [verfasserIn] Peter Arthur-Farraj [verfasserIn] Sergio Velasco-Aviles [verfasserIn] Hugo Cabedo [verfasserIn] Cristina Benito [verfasserIn] Rhona Mirsky [verfasserIn] Kristjan R Jessen [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	nerve regeneration schwann cell c-Jun aging chronic denervation repair cell

Übergeordnetes Werk:	In: eLife - eLife Sciences Publications Ltd, 2013, 10(2021)
Übergeordnetes Werk:	volume:10 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.7554/eLife.62232

Katalog-ID:	DOAJ084208643

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520			\|a After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS.
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spelling	10.7554/eLife.62232 doi (DE-627)DOAJ084208643 (DE-599)DOAJ71cf5cebbc4d40f8b6b3a29c0b196abc DE-627 ger DE-627 rakwb eng QH301-705.5 Laura J Wagstaff verfasserin aut Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS. nerve regeneration schwann cell c-Jun aging chronic denervation repair cell Medicine R Science Q Biology (General) Jose A Gomez-Sanchez verfasserin aut Shaline V Fazal verfasserin aut Georg W Otto verfasserin aut Alastair M Kilpatrick verfasserin aut Kirolos Michael verfasserin aut Liam YN Wong verfasserin aut Ki H Ma verfasserin aut Mark Turmaine verfasserin aut John Svaren verfasserin aut Tessa Gordon verfasserin aut Peter Arthur-Farraj verfasserin aut Sergio Velasco-Aviles verfasserin aut Hugo Cabedo verfasserin aut Cristina Benito verfasserin aut Rhona Mirsky verfasserin aut Kristjan R Jessen verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 10(2021) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:10 year:2021 https://doi.org/10.7554/eLife.62232 kostenfrei https://doaj.org/article/71cf5cebbc4d40f8b6b3a29c0b196abc kostenfrei https://elifesciences.org/articles/62232 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2021
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authorswithroles_txt_mv	Laura J Wagstaff @@aut@@ Jose A Gomez-Sanchez @@aut@@ Shaline V Fazal @@aut@@ Georg W Otto @@aut@@ Alastair M Kilpatrick @@aut@@ Kirolos Michael @@aut@@ Liam YN Wong @@aut@@ Ki H Ma @@aut@@ Mark Turmaine @@aut@@ John Svaren @@aut@@ Tessa Gordon @@aut@@ Peter Arthur-Farraj @@aut@@ Sergio Velasco-Aviles @@aut@@ Hugo Cabedo @@aut@@ Cristina Benito @@aut@@ Rhona Mirsky @@aut@@ Kristjan R Jessen @@aut@@
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callnumber-first	Q - Science
author	Laura J Wagstaff
spellingShingle	Laura J Wagstaff misc QH301-705.5 misc nerve regeneration misc schwann cell misc c-Jun misc aging misc chronic denervation misc repair cell misc Medicine misc R misc Science misc Q misc Biology (General) Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun
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topic_title	QH301-705.5 Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun nerve regeneration schwann cell c-Jun aging chronic denervation repair cell
topic	misc QH301-705.5 misc nerve regeneration misc schwann cell misc c-Jun misc aging misc chronic denervation misc repair cell misc Medicine misc R misc Science misc Q misc Biology (General)
topic_unstemmed	misc QH301-705.5 misc nerve regeneration misc schwann cell misc c-Jun misc aging misc chronic denervation misc repair cell misc Medicine misc R misc Science misc Q misc Biology (General)
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title	Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun
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title_full	Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun
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title_sort	failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring schwann cell c-jun
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title_auth	Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun
abstract	After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS.
abstractGer	After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS.
abstract_unstemmed	After nerve injury, myelin and Remak Schwann cells reprogram to repair cells specialized for regeneration. Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. This provides a molecular framework for addressing important clinical problems, suggesting molecular pathways that can be targeted to promote repair in the PNS.
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title_short	Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun
url	https://doi.org/10.7554/eLife.62232 https://doaj.org/article/71cf5cebbc4d40f8b6b3a29c0b196abc https://elifesciences.org/articles/62232 https://doaj.org/toc/2050-084X
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up_date	2024-07-03T21:45:45.988Z
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Normally providing strong regenerative support, these cells fail in aging animals, and during chronic denervation that results from slow axon growth. This impairs axonal regeneration and causes significant clinical problems. In mice, we find that repair cells express reduced c-Jun protein as regenerative support provided by these cells declines during aging and chronic denervation. In both cases, genetically restoring Schwann cell c-Jun levels restores regeneration to control levels. We identify potential gene candidates mediating this effect and implicate Shh in the control of Schwann cell c-Jun levels. This establishes that a common mechanism, reduced c-Jun in Schwann cells, regulates success and failure of nerve repair both during aging and chronic denervation. 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Failures of nerve regeneration caused by aging or chronic denervation are rescued by restoring Schwann cell c-Jun

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