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Article ; Online: Schwann Cells as Orchestrators of Nerve Repair: Implications for Tissue Regeneration and Pathologies.

Stassart, Ruth M / Gomez-Sanchez, Jose A / Lloyd, Alison C

Cold Spring Harbor perspectives in biology

2024

Abstract: Peripheral nerves exist in a stable state in adulthood providing a rapid bidirectional signaling system to control tissue structure and function. However, following injury, peripheral nerves can regenerate much more effectively than those of the central ... ...

Abstract	Peripheral nerves exist in a stable state in adulthood providing a rapid bidirectional signaling system to control tissue structure and function. However, following injury, peripheral nerves can regenerate much more effectively than those of the central nervous system (CNS). This multicellular process is coordinated by peripheral glia, in particular Schwann cells, which have multiple roles in stimulating and nurturing the regrowth of damaged axons back to their targets. Aside from the repair of damaged nerves themselves, nerve regenerative processes have been linked to the repair of other tissues and de novo innervation appears important in establishing an environment conducive for the development and spread of tumors. In contrast, defects in these processes are linked to neuropathies, aging, and pain. In this review, we focus on the role of peripheral glia, especially Schwann cells, in multiple aspects of nerve regeneration and discuss how these findings may be relevant for pathologies associated with these processes.
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Journal Article
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a041363
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Article ; Online: Schwann cell functions in peripheral nerve development and repair.

Bosch-Queralt, Mar / Fledrich, Robert / Stassart, Ruth M

Neurobiology of disease

2022 Volume 176, Page(s) 105952

Abstract: The glial cell of the peripheral nervous system (PNS), the Schwann cell (SC), counts among the most multifaceted cells of the body. During development, SCs secure neuronal survival and participate in axonal path finding. Simultaneously, they orchestrate ... ...

Abstract	The glial cell of the peripheral nervous system (PNS), the Schwann cell (SC), counts among the most multifaceted cells of the body. During development, SCs secure neuronal survival and participate in axonal path finding. Simultaneously, they orchestrate the architectural set up of the developing nerves, including the blood vessels and the endo-, peri- and epineurial layers. Perinatally, in rodents, SCs radially sort and subsequently myelinate individual axons larger than 1 μm in diameter, while small calibre axons become organised in non-myelinating Remak bundles. SCs have a vital role in maintaining axonal health throughout life and several specialized SC types perform essential functions at specific locations, such as terminal SC at the neuromuscular junction (NMJ) or SC within cutaneous sensory end organs. In addition, neural crest derived satellite glia maintain a tight communication with the soma of sensory, sympathetic, and parasympathetic neurons and neural crest derivatives are furthermore an indispensable part of the enteric nervous system. The remarkable plasticity of SCs becomes evident in the context of a nerve injury, where SC transdifferentiate into intriguing repair cells, which orchestrate a regenerative response that promotes nerve repair. Indeed, the multiple adaptations of SCs are captivating, but remain often ill-resolved on the molecular level. Here, we summarize and discuss the knowns and unknowns of the vast array of functions that this single cell type can cover in peripheral nervous system development, maintenance, and repair.
MeSH term(s)	Humans ; Schwann Cells/metabolism ; Peripheral Nerves/metabolism ; Axons/metabolism ; Neurons/metabolism ; Peripheral Nervous System/metabolism ; Nerve Regeneration/physiology ; Peripheral Nerve Injuries/metabolism
Language	English
Publishing date	2022-12-07
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105952
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Zs.A 4444: Show issues

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Article ; Online: Axo-glial interaction in the injured PNS.

Stassart, Ruth M / Woodhoo, Ashwin

Developmental neurobiology

2020 Volume 81, Issue 5, Page(s) 490–506

Abstract: Axons share a close relationship with Schwann cells, their glial partners in peripheral nerves. An intricate axo-glia network of signals and bioactive molecules regulates the major aspects of nerve development and normal functioning of the peripheral ... ...

Abstract	Axons share a close relationship with Schwann cells, their glial partners in peripheral nerves. An intricate axo-glia network of signals and bioactive molecules regulates the major aspects of nerve development and normal functioning of the peripheral nervous system. Disruptions to these complex axo-glial interactions can have serious neurological consequences, as typically seen in injured nerves. Recent studies in inherited neuropathies have demonstrated that damage to one of the partners in this symbiotic unit ultimately leads to impairment of the other partner, emphasizing the bidirectional influence of axon to glia and glia to axon signaling in these diseases. After physical trauma to nerves, dramatic alterations in the architecture and signaling environment of peripheral nerves take place. Here, axons and Schwann cells respond adaptively to these perturbations and change the nature of their reciprocal interactions, thereby driving the remodeling and regeneration of peripheral nerves. In this review, we focus on the nature and importance of axon-glia interactions in injured nerves, both for the reshaping and repair of nerves after trauma, and in driving pathology in inherited peripheral neuropathies.
MeSH term(s)	Axons/physiology ; Humans ; Nerve Regeneration ; Neuroglia/physiology ; Peripheral Nervous System ; Peripheral Nervous System Diseases ; Schwann Cells/physiology
Language	English
Publishing date	2020-07-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2256184-5
ISSN	1932-846X ; 1097-4695 ; 1932-8451 ; 0022-3034
ISSN (online)	1932-846X ; 1097-4695
ISSN	1932-8451 ; 0022-3034
DOI	10.1002/dneu.22771
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Zs.A 853: Show issues

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Article ; Online: Targeting PI3K/Akt/mTOR signaling in rodent models of PMP22 gene-dosage diseases.

Krauter, Doris / Stausberg, Daniela / Hartmann, Timon J / Volkmann, Stefan / Kungl, Theresa / Rasche, David A / Saher, Gesine / Fledrich, Robert / Stassart, Ruth M / Nave, Klaus-Armin / Goebbels, Sandra / Ewers, David / Sereda, Michael W

EMBO molecular medicine

2024 Volume 16, Issue 3, Page(s) 616–640

Abstract: Haplo-insufficiency of the gene encoding the myelin protein PMP22 leads to focal myelin overgrowth in the peripheral nervous system and hereditary neuropathy with liability to pressure palsies (HNPP). Conversely, duplication of PMP22 causes Charcot-Marie- ...

Abstract	Haplo-insufficiency of the gene encoding the myelin protein PMP22 leads to focal myelin overgrowth in the peripheral nervous system and hereditary neuropathy with liability to pressure palsies (HNPP). Conversely, duplication of PMP22 causes Charcot-Marie-Tooth disease type 1A (CMT1A), characterized by hypomyelination of medium to large caliber axons. The molecular mechanisms of abnormal myelin growth regulation by PMP22 have remained obscure. Here, we show in rodent models of HNPP and CMT1A that the PI3K/Akt/mTOR-pathway inhibiting phosphatase PTEN is correlated in abundance with PMP22 in peripheral nerves, without evidence for direct protein interactions. Indeed, treating DRG neuron/Schwann cell co-cultures from HNPP mice with PI3K/Akt/mTOR pathway inhibitors reduced focal hypermyelination. When we treated HNPP mice in vivo with the mTOR inhibitor Rapamycin, motor functions were improved, compound muscle amplitudes were increased and pathological tomacula in sciatic nerves were reduced. In contrast, we found Schwann cell dedifferentiation in CMT1A uncoupled from PI3K/Akt/mTOR, leaving partial PTEN ablation insufficient for disease amelioration. For HNPP, the development of PI3K/Akt/mTOR pathway inhibitors may be considered as the first treatment option for pressure palsies.
MeSH term(s)	Mice ; Animals ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Rodentia/metabolism ; Charcot-Marie-Tooth Disease/genetics ; Charcot-Marie-Tooth Disease/pathology ; Myelin Proteins/genetics ; Myelin Proteins/metabolism ; TOR Serine-Threonine Kinases ; Arthrogryposis ; Hereditary Sensory and Motor Neuropathy
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Myelin Proteins ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2024-02-21
Publishing country	England
Document type	Journal Article
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.1038/s44321-023-00019-5
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Zs.A 6784: Show issues

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Article ; Online: Axo-glial interdependence in peripheral nerve development.

Fledrich, Robert / Kungl, Theresa / Nave, Klaus-Armin / Stassart, Ruth M

Development (Cambridge, England)

2019 Volume 146, Issue 21

Abstract: During the development of the peripheral nervous system, axons and myelinating Schwann cells form a unique symbiotic unit, which is realized by a finely tuned network of molecular signals and reciprocal interactions. The importance of this complex ... ...

Abstract	During the development of the peripheral nervous system, axons and myelinating Schwann cells form a unique symbiotic unit, which is realized by a finely tuned network of molecular signals and reciprocal interactions. The importance of this complex interplay becomes evident after injury or in diseases in which aspects of axo-glial interaction are perturbed. This Review focuses on the specific interdependence of axons and Schwann cells in peripheral nerve development that enables axonal outgrowth, Schwann cell lineage progression, radial sorting and, finally, formation and maintenance of the myelin sheath.
MeSH term(s)	Animals ; Axons/physiology ; Cell Differentiation ; Cell Lineage ; Cell Separation ; Gene Expression Regulation, Developmental ; Mice ; Myelin Sheath/physiology ; Nerve Regeneration ; Neuroglia/physiology ; Peripheral Nerves/embryology ; Peripheral Nerves/physiology ; Peripheral Nervous System ; Rats ; Schwann Cells/physiology ; Signal Transduction
Language	English
Publishing date	2019-11-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.151704
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Zs.MG 91: Show issues

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Article: Aktuelles zur Charcot-marie-tooth-Erkrankung

Bartl, Michael / Stassart, Ruth M. / Fledrich, Robert / Sereda, Michael W.

Nervenheilkunde

2019 Volume 38, Issue 6, Page(s) 389

Language	German
Document type	Article
ZDB-ID	604504-2
ISSN	0722-1541
Database	Current Contents Medicine

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Article: The Axon-Myelin Unit in Development and Degenerative Disease.

Stassart, Ruth M / Möbius, Wiebke / Nave, Klaus-Armin / Edgar, Julia M

Frontiers in neuroscience

2018 Volume 12, Page(s) 467

Abstract: Axons are electrically excitable, cable-like neuronal processes that relay information between neurons within the nervous system and between neurons and peripheral target tissues. In the central and peripheral nervous systems, most axons over a critical ... ...

Abstract	Axons are electrically excitable, cable-like neuronal processes that relay information between neurons within the nervous system and between neurons and peripheral target tissues. In the central and peripheral nervous systems, most axons over a critical diameter are enwrapped by myelin, which reduces internodal membrane capacitance and facilitates rapid conduction of electrical impulses. The spirally wrapped myelin sheath, which is an evolutionary specialisation of vertebrates, is produced by oligodendrocytes and Schwann cells; in most mammals myelination occurs during postnatal development and after axons have established connection with their targets. Myelin covers the vast majority of the axonal surface, influencing the axon's physical shape, the localisation of molecules on its membrane and the composition of the extracellular fluid (in the periaxonal space) that immerses it. Moreover, myelinating cells play a fundamental role in axonal support, at least in part by providing metabolic substrates to the underlying axon to fuel its energy requirements. The unique architecture of the myelinated axon, which is crucial to its function as a conduit over long distances, renders it particularly susceptible to injury and confers specific survival and maintenance requirements. In this review we will describe the normal morphology, ultrastructure and function of myelinated axons, and discuss how these change following disease, injury or experimental perturbation, with a particular focus on the role the myelinating cell plays in shaping and supporting the axon.
Language	English
Publishing date	2018-07-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2018.00467
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Article: Aktuelles zur Charcot-Marie-Tooth-Erkrankung

Bartl, Michael / Stassart, Ruth M. / Fledrich, Robert / Sereda, Michael W.

Nervenheilkunde

2019 Volume 38, Issue 06, Page(s) 389–396

Abstract: Die Charcot-Marie-Tooth-Erkrankung (CMT) ist die häufigste hereditäre Neuropathie (Prävalenz 1:2500) mit über 90 assoziierten Genen. Der häufigste Subtyp (CMT1A), assoziiert mit einer Duplikation des peripheren Myelinprotein-22-Gens (PMP22) ist Ursache ... ...

Abstract	Die Charcot-Marie-Tooth-Erkrankung (CMT) ist die häufigste hereditäre Neuropathie (Prävalenz 1:2500) mit über 90 assoziierten Genen. Der häufigste Subtyp (CMT1A), assoziiert mit einer Duplikation des peripheren Myelinprotein-22-Gens (PMP22) ist Ursache für 40–50 % aller Fälle. Klinische Zeichen sind distal symmetrische Paresen, Atrophien, Sensibilitätsstörungen, Fußdeformitäten und Areflexie. Validierte Skalen zur Evaluation der Beeinträchtigung (CMTNS2, ONLS, 9-hole-pegtest, Gehtestungen) sind verfügbar und molekulare Biomarker aus Blut und Hautbiopsien wurden validiert. Therapieoptionen im Entwicklungsstadium sind das Gen-Silencing (Minderung der Überexpression von PMP22), Sekretasen zur Regulierung der Neuregulinaktivität mit Einfluss auf Meylindicke und Funktion sowie Inhibitoren des Kalziuminfluxes in Schwannzellen. PXT3003 (Sorbitol, Naltrexon, Baclofen) wurde im Tiermodell erfolgreich getestet. Ein möglicher Therapieansatz mittels Substitution des Fettmoleküls Lecithin konnte in CMT1A-Ratten die Muskelkraft und die Anzahl myelinisierter Axone erhöhen.
Keywords	Charcot-Marie-Tooth ; Neurogenetik ; Hereditäre Neuropathie ; Biomarker ; Charcot-Marie-Tooth ; neurogenetics ; hereditary neuropathy ; biomarker
Language	German
Publishing date	2019-06-01
Publisher	© Georg Thieme Verlag KG Stuttgart · New York
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	2223503-6
ISSN	2567-5788 ; 0722-1541
ISSN (online)	2567-5788
ISSN	0722-1541
DOI	10.1055/a-0883-9906
Database	Thieme publisher's database

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Article ; Online: Myelin insulation as a risk factor for axonal degeneration in autoimmune demyelinating disease.

Schäffner, Erik / Bosch-Queralt, Mar / Edgar, Julia M / Lehning, Maria / Strauß, Judith / Fleischer, Niko / Kungl, Theresa / Wieghofer, Peter / Berghoff, Stefan A / Reinert, Tilo / Krueger, Martin / Morawski, Markus / Möbius, Wiebke / Barrantes-Freer, Alonso / Stieler, Jens / Sun, Ting / Saher, Gesine / Schwab, Markus H / Wrede, Christoph /

Frosch, Maximilian / Prinz, Marco / Reich, Daniel S / Flügel, Alexander / Stadelmann, Christine / Fledrich, Robert / Nave, Klaus-Armin / Stassart, Ruth M

Nature neuroscience

2023 Volume 26, Issue 7, Page(s) 1218–1228

Abstract: Axonal degeneration determines the clinical outcome of multiple sclerosis and is thought to result from exposure of denuded axons to immune-mediated damage. Therefore, myelin is widely considered to be a protective structure for axons in multiple ... ...

Abstract	Axonal degeneration determines the clinical outcome of multiple sclerosis and is thought to result from exposure of denuded axons to immune-mediated damage. Therefore, myelin is widely considered to be a protective structure for axons in multiple sclerosis. Myelinated axons also depend on oligodendrocytes, which provide metabolic and structural support to the axonal compartment. Given that axonal pathology in multiple sclerosis is already visible at early disease stages, before overt demyelination, we reasoned that autoimmune inflammation may disrupt oligodendroglial support mechanisms and hence primarily affect axons insulated by myelin. Here, we studied axonal pathology as a function of myelination in human multiple sclerosis and mouse models of autoimmune encephalomyelitis with genetically altered myelination. We demonstrate that myelin ensheathment itself becomes detrimental for axonal survival and increases the risk of axons degenerating in an autoimmune environment. This challenges the view of myelin as a solely protective structure and suggests that axonal dependence on oligodendroglial support can become fatal when myelin is under inflammatory attack.
MeSH term(s)	Mice ; Animals ; Humans ; Myelin Sheath/metabolism ; Axons/metabolism ; Multiple Sclerosis/pathology ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Risk Factors
Language	English
Publishing date	2023-06-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-023-01366-9
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: Adipo-glial signaling mediates metabolic adaptation in peripheral nerve regeneration.

Sundaram, Venkat Krishnan / Schütza, Vlad / Schröter, Nele H / Backhaus, Aline / Bilsing, Annika / Joneck, Lisa / Seelbach, Anna / Mutschler, Clara / Gomez-Sanchez, Jose A / Schäffner, Erik / Sánchez, Eva Ernst / Akkermann, Dagmar / Paul, Christina / Schwagarus, Nancy / Müller, Silvana / Odle, Angela / Childs, Gwen / Ewers, David / Kungl, Theresa /

Sitte, Maren / Salinas, Gabriela / Sereda, Michael W / Nave, Klaus-Armin / Schwab, Markus H / Ost, Mario / Arthur-Farraj, Peter / Stassart, Ruth M / Fledrich, Robert

Cell metabolism

2023 Volume 35, Issue 12, Page(s) 2136–2152.e9

Abstract: The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin ... ...

Abstract	The peripheral nervous system harbors a remarkable potential to regenerate after acute nerve trauma. Full functional recovery, however, is rare and critically depends on peripheral nerve Schwann cells that orchestrate breakdown and resynthesis of myelin and, at the same time, support axonal regrowth. How Schwann cells meet the high metabolic demand required for nerve repair remains poorly understood. We here report that nerve injury induces adipocyte to glial signaling and identify the adipokine leptin as an upstream regulator of glial metabolic adaptation in regeneration. Signal integration by leptin receptors in Schwann cells ensures efficient peripheral nerve repair by adjusting injury-specific catabolic processes in regenerating nerves, including myelin autophagy and mitochondrial respiration. Our findings propose a model according to which acute nerve injury triggers a therapeutically targetable intercellular crosstalk that modulates glial metabolism to provide sufficient energy for successful nerve repair.
MeSH term(s)	Peripheral Nerves ; Myelin Sheath/metabolism ; Neuroglia ; Schwann Cells/metabolism ; Nerve Regeneration/physiology
Language	English
Publishing date	2023-11-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.10.017
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