Neuregulin/erbB signaling is critically required for survival and proliferation of Schwann cells as well as for establishing correct myelin thickness of peripheral nerves during development. In this study, we investigated whether erbB2 signaling in Schwann cells is also essential for the maintenance of myelinated peripheral nerves and for Schwann cell proliferation and survival after nerve injury. To this end, we used inducible Cre-loxP technology using a PLP-CreERT2 allele to ablate erbB2 in adult Schwann cells. ErbB2 expression was markedly reduced after induction of erbB2 gene disruption with no apparent effect on the maintenance of already established myelinated peripheral nerves. In contrast to development, Schwann cell proliferation and survival were not impaired in mutant animals after nerve injury, despite reduced levels of MAPK-P (phosphorylated mitogen-activated protein kinase) and cyclin D1. ErbB1 and erbB4 do not compensate for the loss of erbB2. We conclude that adult Schwann cells do not require major neuregulin signaling through erbB2 for proliferation and survival after nerve injury, in contrast to development and in cell culture.
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http://dx.doi.org/10.1523/JNEUROSCI.4594-05.2006 | DOI Listing |
Commun Biol
January 2025
Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Histological chorioamnionitis (HCA) is a form of maternal immune activation (MIA) linked to an increased risk of neurodevelopmental disorders in offspring. Our previous study identified neurodevelopmental impairments in an MIA mouse model mimicking HCA. Thus, this study investigated the role of CD11c microglia, key contributors to myelination through IGF-1 production, in this pathology.
View Article and Find Full Text PDFActa Biomater
January 2025
Central laboratory of Liaocheng People's Hospital, Liaocheng, Shandong, 252000, China. Electronic address:
Peripheral nerve injury (PNI) as a common clinical issue that presents significant challenges for repair. Factors such as donor site morbidity from autologous transplantation, slow recovery of long-distance nerve damage, and deficiencies in local cytokines and extracellular matrix contribute to the complexity of effective PNI treatment. It is extremely urgent to develop functional nerve guidance conduits (NGCs) as substitutes for nerve autografts.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Laboratory for Functional Imaging & Research on Stem Cells, BIOMED, Faculty of Medicine and Life Sciences, Hasselt University, Diepenbeek, Belgium. Electronic address:
Charcot-Marie-Tooth disease type 1A (CMT1A) is an inherited peripheral neuropathy caused by a duplication of the peripheral myelin protein 22 (PMP22) gene. It is primarily marked by Schwann cell dedifferentiation and demyelination, leading to motor and sensory deficits. Cyclic adenosine monophosphate (cAMP) is crucial for Schwann cell differentiation and maturation.
View Article and Find Full Text PDFACS Appl Bio Mater
January 2025
Institute of Physics and Materials Science, Department of Natural Sciences and Sustainable Ressources, BOKU University, Peter Jordan-Straß 82, 1190 Vienna, Austria.
Spider silk (SPSI) is a promising candidate for use as a filler material in nerve guidance conduits (NGCs), facilitating peripheral nerve regeneration by providing a scaffold for Schwann cells (SCs) and axonal growth. However, the specific properties of SPSI that contribute to its regenerative success remain unclear. In this study, the egg sac silk of is investigated, which contains two distinct fiber types: tubuliform (TU) and major ampullate (MA) silk.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Cell and Developmental Biology, University of Colorado School of Medicine, Aurora, CO, USA.
Myelin loss induces neural dysfunction and contributes to the pathophysiology of neurodegenerative diseases, injury conditions, and aging. Because remyelination is often incomplete, better understanding endogenous remyelination and developing remyelination therapies that restore neural function are clinical imperatives. Here, we use in vivo two-photon microscopy and electrophysiology to study the dynamics of endogenous and therapeutic-induced cortical remyelination and functional recovery after cuprizone-mediated demyelination in mice.
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