ArticleMolecular brain2021
GDF11 expressed in the adult brain negatively regulates hippocampal neurogenesis.
Article in Molecular brain, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Blood-based therapies to combat neurodegenerative diseases.Metabolic brain disease · 2024Review
- GDF11 and aging biology - controversies resolved and pending.The journal of cardiovascular aging · 2023Article
- Blood-to-brain communication in aging and rejuvenation.Nature neuroscience · 2023Review
- MeCP2 regulateseLife · 2023Article
- Systemic GDF11 attenuates depression-like phenotype in aged mice via stimulation of neuronal autophagy.Nature aging · 2023Article
- GDF11 reverses mood and memory declines in aging.Nature aging · 2023Article
- GDF11 Regulates PC12 Neural Stem Cells via ALK5-Dependent PI3K-Akt Signaling Pathway.International journal of molecular sciences · 2022Article
- The emerging translational potential of GDF11 in chronic wound healing.Journal of orthopaedic translation · 2022Review
- Regulation of Myostatin on the Growth and Development of Skeletal Muscle.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth differentiation factor 11 (GDF11) is a transforming factor-β superfamily member that functions as a negative regulator of neurogenesis during embryonic development. However, when recombinant GDF11 (rGDF11) is administered systemically in aged mice, it promotes neurogenesis, the opposite of its role during development. The goal of the present study was to reconcile this apparent discrepancy by performing the first detailed investigation into the expression of endogenous GDF11 in the adult brain and its effects on neurogenesis. Using quantitative histological analysis, we observed that Gdf11 is most highly expressed in adult neurogenic niches and non-neurogenic regions within the hippocampus, choroid plexus, thalamus, habenula, and cerebellum. To investigate the role of endogenous GDF11 during adult hippocampal neurogenesis, we generated a tamoxifen inducible mouse that allowed us to reduce GDF11 levels. Depletion of Gdf11 during adulthood increased proliferation of neural progenitors and decreased the number of newborn neurons in the hippocampus, suggesting that endogenous GDF11 remains a negative regulator of hippocampal neurogenesis in adult mice. These findings further support the idea that circulating systemic GDF11 and endogenously expressed GDF11 in the adult brain have different target cells or mechanisms of action. Our data describe a role for GDF11-dependent signaling in adult neurogenesis that has implications for how GDF11 may be used to treat CNS disease.
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Registered trials
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