ArticleProceedings of the National Academy of Sciences of the United States of America2006
Purinergic signaling induces thrombospondin-1 expression in astrocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 100 citations in OpenAlex.
- CD47 and thrombospondin-1 contribute to immune evasion byProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Purinergic Signalling Mediates Aberrant Excitability of Developing Neuronal Circuits in the Fmr1 Knockout Mouse Model.Molecular neurobiology · 2024Article
- Increased thrombospondin-1 levels contribute to epileptic susceptibility in neonatal hyperthermia without seizures via altered synaptogenesis.Cell death discovery · 2024Article
- Synaptogenesis by Cholinergic Stimulation of Astrocytes.Neurochemical research · 2023Article
- Synaptogenesis by Cholinergic Stimulation of Astrocytes.Research square · 2023Article
- Müller Glia in Retinal Development: From Specification to Circuit Integration.Frontiers in neural circuits · 2021Review
- Astrocyte-Neuron Signaling in Synaptogenesis.Frontiers in cell and developmental biology · 2021Review
- Age-dependent decline in neurogenesis of the hippocampus and extracellular nucleotides.Human cell · 2019Review
- Astrocyte Mechano-Activation by High-Rate Overpressure Involves Alterations in Structural and Junctional Proteins.Frontiers in neurology · 2019Article
- Thrombospondin-1 Is Necessary for the Development and Repair of Corneal Nerves.International journal of molecular sciences · 2018Article
- Contributions of monocytes to nervous system disorders.Journal of molecular medicine (Berlin, Germany) · 2018Review
- VEGF-A inhibits agonist-mediated CaThe Journal of physiology · 2018Article
- A Purinergic P2 Receptor Family-Mediated Increase in Thrombospondin-1 Bolsters Synaptic Density and Epileptic Seizure Activity in the Amygdala-Kindling Rat Model.Frontiers in cellular neuroscience · 2018Article
- Glial responses to implanted electrodes in the brain.Nature biomedical engineering · 2017Article
- Cell Biology of Astrocyte-Synapse Interactions.Neuron · 2017Review
- Role of Matricellular Proteins in Disorders of the Central Nervous System.Neurochemical research · 2017Review
- Article
- Spinal Astrocytic Thrombospondin-4 Induced by Excitatory Neuronal Signaling Mediates Pain After Facet Capsule Injury.Annals of biomedical engineering · 2016Article
- "Targeting astrocytes in CNS injury and disease: A translational research approach".Progress in neurobiology · 2016Review
- How Does Transcranial Magnetic Stimulation Influence Glial Cells in the Central Nervous System?Frontiers in neural circuits · 2016Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
Thrombospondin (TSP)-1, a multidomain glycoprotein, is secreted from astrocytes and promotes synaptogenesis. However, little is known about the mechanisms regulating its expression and release. In this article, we report that purinergic signaling participates in the production and secretion of TSP-1. Treatment of primary cultures of rat cortical astrocytes with extracellular ATP caused an increase in TSP-1 expression in a time- and concentration-dependent manner and was inhibited by antagonists of P2 and P1 purinergic receptors. Agonist studies revealed that UTP, but not 2',3'-O-(4-benzoyl)benzoyl-ATP, 2-methylthio-ADP, adenosine, or 5'-N-ethyl-carboxamidoadenosine, caused a significant increase in TSP-1 expression. In addition, release of TSP-1 was stimulated by ATP and UTP but not by 2-methylthio-ADP or adenosine. Additional studies indicated that P2Y(4) receptors stimulate both TSP-1 expression and release. P2Y receptors are coupled to protein kinase cascades, and signaling studies demonstrated that blockade of mitogen-activated protein kinases or Akt inhibited ATP- and UTP-induced TSP-1 expression. Using an in vitro model of CNS trauma that stimulates release of ATP, we found that TSP-1 expression increased after mechanical strain and was completely blocked by a P2 receptor antagonist and by inhibition of p38/mitogen-activated protein kinase and Akt, thereby indicating a major role for P2 receptor/protein kinase signaling in TSP-1 expression induced by trauma. We conclude that TSP-1 expression can be regulated by activation of P2Y receptors, particularly P2Y(4), coupled to protein kinase signaling pathways and suggest that purinergic signaling may be an important factor in TSP-1-mediated cell-matrix and cell-cell interactions such as those occurring during development and repair.
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