ArticleScientific reports2019
ALK4/5-dependent TGF-β signaling contributes to the crosstalk between neurons and microglia following axonal lesion.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Notch signaling in leech neurogenesis: expression patterns and functional insights in the Glossiphoniid leechAnimal cells and systems · 2026Article
- The Yin and Yang of Microglia-Derived Extracellular Vesicles in CNS Injury and Diseases.Cells · 2024Review
- Microglial Transforming Growth Factor-β Signaling in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- Characterization of the roles of amphiregulin and transforming growth factor β1 in microvasculature-like formation in human granulosa-lutein cells.Frontiers in cell and developmental biology · 2022Article
- The Potential Role of Dysfunctions in Neuron-Microglia Communication in the Pathogenesis of Brain Disorders.Current neuropharmacology · 2020Review
- Isolation of microglia-derived extracellular vesicles: towards miRNA signatures and neuroprotection.Journal of nanobiotechnology · 2019Article
- Management of herpes zoster in Ayurveda through medicinal leeches and other composite Ayurveda Treatment.Journal of Ayurveda and integrative medicineArticle
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuronal activity is closely influenced by glia, especially microglia which are the resident immune cells in the central nervous system (CNS). Microglia in medicinal leech are the only cells able to migrate to the injury site within the 24 hours post-lesion. The microglia-neuron interactions constitute an important mechanism as there is neither astrocyte nor oligodendrocyte in the leech CNS. Given that axonal sprouting is impaired when microglia recruitment is inhibited, the crosstalk between microglia and neurons plays a crucial role in neuroprotection. The present results show that neurons and microglia both use ALK4/5 (a type of TGF-β receptor) signaling in order to maintain mutual exchanges in an adult brain following an axonal injury. Indeed, a TGF-β family member (nGDF) is immediately released by injured axons contributing to the early recruitment of ALK4/5
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