ArticleThe Journal of biological chemistry2015
Nuclear Calcium Buffering Capacity Shapes Neuronal Architecture.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Beyond vessels: unraveling the impact of VEGFs on neuronal functions and structure.Journal of biomedical science · 2025Review
- VEGFD signaling balances stability and activity-dependent structural plasticity of dendrites.Cellular and molecular life sciences : CMLS · 2024Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Interleukin-13 and its receptor are synaptic proteins involved in plasticity and neuroprotection.Nature communications · 2023Article
- Neuronal nuclear calcium signaling suppression of microglial reactivity is mediated by osteoprotegerin after traumatic brain injury.Journal of neuroinflammation · 2022Article
- Npas4 regulates medium spiny neuron physiology and gates cocaine-induced hyperlocomotion.EMBO reports · 2021Article
- RyR-mediated CaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Abnormalities of synaptic mitochondria in autism spectrum disorder and related neurodevelopmental disorders.Journal of molecular medicine (Berlin, Germany) · 2021Review
- VEGFD Protects Retinal Ganglion Cells and, consequently, Capillaries against Excitotoxic Injury.Molecular therapy. Methods & clinical development · 2020Article
- Nasally delivered VEGFD mimetics mitigate stroke-induced dendrite loss and brain damage.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Functional Consequences of Calcium-Dependent Synapse-to-Nucleus Communication: Focus on Transcription-Dependent Metabolic Plasticity.Cold Spring Harbor perspectives in biology · 2020Review
- Mimicking Age-Associated Gadd45γ Dysregulation Results in Memory Impairments in Young Adult Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Genetically Encoded Calcium Indicators Can Impair Dendrite Growth of Cortical Neurons.Frontiers in cellular neuroscience · 2020Article
- Self-organization of modular network architecture by activity-dependent neuronal migration and outgrowth.eLife · 2019Article
- Histone deacetylase 4 shapes neuronal morphology via a mechanism involving regulation of expression of vascular endothelial growth factor D.The Journal of biological chemistry · 2018Article
- Alpha-synuclein aggregates activate calcium pump SERCA leading to calcium dysregulation.EMBO reports · 2018Article
- Emerging Roles for VEGF-D in Human Disease.Biomolecules · 2018Review
- Reciprocal Interaction of Dendrite Geometry and Nuclear Calcium-VEGFD Signaling Gates Memory Consolidation and Extinction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Therapeutic targeting of the pathological triad of extrasynaptic NMDA receptor signaling in neurodegenerations.The Journal of experimental medicine · 2017Review
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium-binding proteins (CaBPs) such as parvalbumin are part of the cellular calcium buffering system that determines intracellular calcium diffusion and influences the spatiotemporal dynamics of calcium signals. In neurons, CaBPs are primarily localized to the cytosol and function, for example, in nerve terminals in short-term synaptic plasticity. However, CaBPs are also expressed in the cell nucleus, suggesting that they modulate nuclear calcium signals, which are key regulators of neuronal gene expression. Here we show that the calcium buffering capacity of the cell nucleus in mouse hippocampal neurons regulates neuronal architecture by modulating the expression levels of VEGFD and the complement factor C1q-c, two nuclear calcium-regulated genes that control dendrite geometry and spine density, respectively. Increasing the levels of nuclear calcium buffers by means of expression of a nuclearly targeted form of parvalbumin fused to mCherry (PV.NLS-mC) led to a reduction in VEGFD expression and, as a result, to a decrease in total dendritic length and complexity. In contrast, mRNA levels of the synapse pruning factor C1q-c were increased in neurons expressing PV.NLS-mC, causing a reduction in the density and size of dendritic spines. Our results establish a close link between nuclear calcium buffering capacity and the transcription of genes that determine neuronal structure. They suggest that the development of cognitive deficits observed in neurological conditions associated with CaBP deregulation may reflect the loss of necessary structural features of dendrites and spines.
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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.