ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Expression of neuregulins and their putative receptors, ErbB2 and ErbB3, is induced during Wallerian degeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
102 citing papers in PubMed, 328 citations in OpenAlex.
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- Primary Cilia in Glial Cells: An Oasis in the Journey to Overcoming Neurodegenerative Diseases.Frontiers in neuroscience · 2021Review
- Mechanisms of Schwann cell plasticity involved in peripheral nerve repair after injury.Cellular and molecular life sciences : CMLS · 2020Review
- Disease propagation in amyotrophic lateral sclerosis (ALS): an interplay between genetics and environment.Journal of neuroinflammation · 2020Review
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- Evaluation of two methods to isolate Schwann cells from murine sciatic nerve.Journal of neuroscience methods · 2020Article
- Partial enzyme digestion facilitates regeneration of crushed nerve in rat.Translational neuroscience · 2020Article
- RalGTPases contribute to Schwann cell repair after nerve injury via regulation of process formation.The Journal of cell biology · 2019Article
- The Complex Work of Proteases and Secretases in Wallerian Degeneration: Beyond Neuregulin-1.Frontiers in cellular neuroscience · 2019Review
- The Success and Failure of the Schwann Cell Response to Nerve Injury.Frontiers in cellular neuroscience · 2019Review
- Polycomb repression regulates Schwann cell proliferation and axon regeneration after nerve injury.Glia · 2018Article
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schwann cell dedifferentiation and proliferation is a prerequisite to axonal regeneration in the injured peripheral nervous system. The neuregulin (NRG) family of growth and differentiation factors may play a particularly important role in this process, because these axon-associated molecules are potent Schwann cell mitogens and differentiation factors in vitro. We have examined Schwann cell DNA synthesis and the expression of NRGs and their receptors, the erbB membrane tyrosine kinases, in rat sciatic nerve, sensory ganglia, and spinal cord 0-30 d postaxotomy. Analysis of NRG cDNAs from these tissues revealed several novel splice variants and showed that cells endogenous to injured nerve express NRG mRNAs. A selective induction of mRNAs encoding the glial growth factor (GGF) subfamily of NRGs occurs in nerve beginning 3 d postaxotomy and thus coincides with the onset of Schwann cell DNA synthesis. In later stages of Wallerian degeneration, however, Schwann cell mitogenesis markedly decreases, whereas elevated GGF expression persists. Of the four known erbB kinases, Schwann cells express both erbB2 and erbB3 receptors over the entire interval studied. Expression of erbB2 and erbB3 is coordinately induced in response to axotomy, indicating that Schwann cell responses to NRGs may be modulated by changes in receptor density. Neuregulin (including transmembrane precursors) and erbB protein are associated with Schwann cells postaxotomy. Thus, in contrast to the concept of NRGs as axon-associated mitogens, our findings suggest that NRGs produced by Schwann cells themselves may be partially responsible for Schwann cell proliferation during Wallerian degeneration, probably acting via autocrine or paracrine mechanisms.
Indexed as
Identifiers
9030624PMC6573392W1515977320What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.