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We began analyzing https://www.nature.com/articles/nn.3560, but it redirected us to https://www.nature.com/articles/nn.3560. The analysis below is for the second page.

Title[redir]:
RETRACTED ARTICLE: TGF-β signaling regulates neuronal C1q expression and developmental synaptic refinement | Nature Neuroscience
Description:
In this study, the authors show that, during the retinogeniculate refinement period, astrocyte-derived TGF-β regulates the expression and synaptic localization of C1q, a classical complement protein. They find that TGF-β signaling and C1q expression in neurons are key regulators of microglia-mediated synaptic pruning in the dorsal lateral geniculate nucleus. 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.

Matching Content Categories {📚}

  • Education
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Content Management System {📝}

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Custom-built

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Traffic Estimate {📈}

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

pubmed, google, scholar, cas, central, retinal, nature, microglia, tgfβ, expression, article, mice, neurosci, data, synaptic, signaling, rgcs, cell, tgfβrii, mouse, anova, growth, access, bar, fig, developing, development, neuron, supplementary, cells, synapse, scale, content, analysis, neuronal, complement, ganglion, transforming, twoway, shows, source, refinement, stevens, synapses, factor, neurons, cns, biol, axon, cookies,

Topics {✒️}

nature portfolio privacy policy advertising anti-tgf-β injected mice glia-secreted tgf-β ligand social media nature 308 nature 486 nature 389 nature transforming growth factor-β1 author information authors facilitating tgf-β signaling data implicate tgf-β anti-tgf-β injected tgf-β-dependent gene author correspondence innate immune cells microglia-mediated synaptic pruning anti-c1q antibody production retinal ganglion cells tgf-β signaling acm-induced c1q upregulation content retracted article springerlink instant access modulates synaptic depression c3-dependent microglial phagocytosis anti-tgf-β complement-dependent synapse elimination regulates axon pruning central synapse function ganglion cell layer classical complement cascade performed data analysis amacrine interneuron development astrocyte-derived factor regulating microglial phagocytosis neuronal c1q expression astrocyte-induced synaptogenesis microglia activation state synchronous bmp inhibition developmental synaptic refinement tgf-β3 mrna privacy immunoglobulin superfamily protein regulating trio expression anti-βiv spectrin cytokine tgf-β1 complement-dependent manner institutional subscriptions read

Schema {🗺️}

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         description:In this study, the authors show that, during the retinogeniculate refinement period, astrocyte-derived TGF-β regulates the expression and synaptic localization of C1q, a classical complement protein. They find that TGF-β signaling and C1q expression in neurons are key regulators of microglia-mediated synaptic pruning in the dorsal lateral geniculate nucleus. 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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         dateModified:2022-01-13T00:00:00Z
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      description:In this study, the authors show that, during the retinogeniculate refinement period, astrocyte-derived TGF-β regulates the expression and synaptic localization of C1q, a classical complement protein. They find that TGF-β signaling and C1q expression in neurons are key regulators of microglia-mediated synaptic pruning in the dorsal lateral geniculate nucleus. 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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         Animal Genetics and Genomics
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