ArticleExperimental neurology2017
TNF superfamily member APRIL enhances midbrain dopaminergic axon growth and contributes to the nigrostriatal projection in vivo.
Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
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- Bioinformatics analysis of potential common pathogenic mechanism for carotid atherosclerosis and Parkinson's disease.Frontiers in aging neuroscience · 2023Article
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- How CD40L reverse signaling regulates axon and dendrite growth.Cellular and molecular life sciences : CMLS · 2021Article
- CD40 forward signalling is a physiological regulator of early sensory axon growth.Development (Cambridge, England) · 2019Article
- Regional Differences in the Contributions of TNF Reverse and Forward Signaling to the Establishment of Sympathetic Innervation.Developmental neurobiology · 2019Article
- TWE-PRIL reverse signalling suppresses sympathetic axon growth and tissue innervation.Development (Cambridge, England) · 2018Article
- Phosphorylation of Parkin at serine 65 is essential for its activationOpen biology · 2018Article
- CD40 is a major regulator of dendrite growth from developing excitatory and inhibitory neurons.eLife · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have studied the role of the tumor necrosis factor superfamily member APRIL in the development of embryonic mouse midbrain dopaminergic neurons in vitro and in vivo. In culture, soluble APRIL enhanced axon growth during a window of development between E12 and E14 when nigrostriatal axons are growing to their targets in the striatum in vivo. April transcripts were detected in both the striatum and midbrain during this period and at later stages. The axon growth-enhancing effect of APRIL was similar to that of glial cell-derived neurotrophic factor (GDNF), but in contrast to GDNF, APRIL did not promote the survival of midbrain dopaminergic neurons. The effect of APRIL on axon growth was prevented by function-blocking antibodies to one of its receptors, BCMA (TNFRSF13A), but not by function-blocking antibodies to the other APRIL receptor, TACI (TNFRSF13B), suggesting that the effects of APRIL on axon growth are mediated by BCMA. In vivo, there was a significant reduction in the density of midbrain dopaminergic projections to the striatum in April-/- embryos compared with wild type littermates at E14. These findings demonstrate that APRIL is a physiologically relevant factor for the nigrostriatal projection. Given the importance of the degeneration of dopaminergic nigrostriatal connections in the pathogenesis and progression of Parkinson's disease, our findings contribute to our understanding of the factors that establish nigrostriatal integrity.
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