RETRACTED ARTICLE: TGF-β signaling regulates neuronal C1q expression and developmental synaptic refinement
Open accessAbstract
Immune molecules, including complement proteins C1q and C3, have emerged as critical mediators of synaptic refinement and plasticity. Complement localizes to synapses and refines the developing visual system through C3-dependent microglial phagocytosis of synapses. Retinal ganglion cells (RGCs) express C1q, the initiating protein of the classical complement cascade, during retinogeniculate refinement; however, the signals controlling C1q expression and function remain elusive. Previous work implicated an astrocyte-derived factor in regulating neuronal C1q expression. Here we identify retinal transforming growth factor (TGF)-β as a key regulator of neuronal C1q expression and synaptic pruning in the developing visual system. Mice lacking TGF-β receptor II (TGFβRII) in retinal neurons had reduced C1q expression in RGCs and reduced synaptic localization of complement, and phenocopied refinement defects observed in complement-deficient mice, including reduced eye-specific segregation and microglial engulfment of RGC inputs. These data implicate TGF-β in regulating neuronal C1q expression to initiate complement- and microglia-mediated synaptic pruning.
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During development, C1q and C3 localize to synapses and mediate synapse elimination by phagocytic microglia.
“During development, C1q and C3 localize to synapses and mediate synapse elimination by phagocytic microglia (5-7).”
From Complement and microglia mediate early synapse loss in Alzheimer mouse models (2016) · cites this paper as [7]
Astrocytes eliminate excess synapses by phagocytosis using the receptors Mertk and Megf10 and indirectly by inducing expression of complement cascade components in neurons.
“and by eliminating excess synapses by phagocytosis using the receptors Mertk and Megf10 and indirectly by inducing expression of complement cascade components in neurons (Bialas and Stevens, 2013; Chung et al., 2013; Stevens et al., 2007).”
From The aging astrocyte transcriptome from multiple regions of the mouse brain. (2018) · cites this paper as Bialas and Stevens, 2013
Microglia can be primed early in development, like peripheral macrophages.
“microglia, like their macrophage relatives in the periphery, can be primed early in development223.”
From Immune mediators in the brain and peripheral tissues in autism spectrum disorder (2015) · cites this paper as [223]
Microglia play a crucial role in synaptic and axonal pruning during development by phagocytizing inappropriate synaptic connections and axons, shaping neural circuits.
“Microglia play a crucial role in synaptic and axonal pruning during development by phagocytizing inappropriate synaptic connections and axons, thereby shaping neural circuits in the developing brain41,88–90.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [88]
Astrocytic secretion of TGF-β regulates complement expression to initiate microglia to begin synaptic elimination.
“Astrocytic secretion of TGF-β regulates complement expression to initiate microglia to begin synaptic elimination (Bialas and Stevens, 2013).”
From Adult neurogenesis, glia, and the extracellular matrix (2019) · cites this paper as Bialas and Stevens, 2013
Astrocyte-microglia communication dictates which synaptic elements should be pruned during thalamo-cortical network refinement.
“evidence suggesting that astrocyte–microglia communication dictates which synaptic elements should be pruned during thalamo–cortical network refinement,56”
From Microglial P2Y12 is necessary for synaptic plasticity in mouse visual cortex (2016) · cites this paper as [56]
In the healthy adult brain, complement components are downregulated; however, in aging brains, C1q and C3 are highly upregulated and deposited on synapses, particularly in the hippocampus, the most vulnerable region in synapse loss in AD.
“In the healthy adult brain, these complement components are downregulated. However, in aging brains, C1q and C3 are highly upregulated and are deposited on synapses, particularly in the hippocampus, the most vulnerable region in the synapse loss in AD (Bialas and Stevens, 2013).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Bialas and Stevens, 2013
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- Authors
- Bialas, A. R., & Stevens, B.
- Affiliations
- Boston Children's Hospital (US)
- Corresponding author
- Stevens, Beth
- ORCID
- Stevens, Beth
- Venue
- Nature Neuroscience
- Published
- 2013-10-27
- Volume
- 16
- Issue
- 12
- Pages
- 1773-1782
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC3973738
- OpenAlex
- W2151498098
- Cited by
- 519
- References
- 51
- Citations by year
- 2026: 5 · 2025: 6 · 2024: 16 · 2023: 19 · 2022: 31 · 2021: 80 · 2020: 74 · 2019: 58 · 2018: 62 · 2017: 46 · 2016: 40 · 2015: 42 · 2014: 36 · 2013: 4
- FWCI
- 22.82
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- retraction (2022-01-13)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- National Institute on Drug Abuse (R01DA015043, R01-DA-15043)
- National Institute of Neurological Disorders and Stroke (R01-NS-07100801, R01NS071008)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P30HD018655, P30HD-18655)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- TGF-beta signaling, C1q, complement system, synaptic pruning, dorsal lateral geniculate nucleus, microglia, retinal ganglion cells, TGF-βRII, visual system development, eye-specific segregation
- MeSH terms
- Receptor, Transforming Growth Factor-beta Type II, Age Factors, Animals, Animals, Newborn, Cell Count, Cells, Cultured, Cerebral Cortex, Mice, Inbred C57BL, Mice, Transgenic, Neuroglia, Retina, Retinal Ganglion Cells, Synapses, Transcription Factors, Signal Transduction, Complement C1q, Transforming Growth Factor beta, Rats, Sprague-Dawley, Protein Serine-Threonine Kinases, Receptors, Transforming Growth Factor beta, Homeodomain Proteins, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Mice, Rats
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