Thrombospondins are astrocyte-secreted proteins that promote CNS synaptogenesis.

By K. S. Christopherson, E. Ullian, C. Stokes, C. Mullowney, J. Hell, A. Agah, J. Lawler, D. Mosher, P. Bornstein, B. Barres. Cell, 2005

1,692 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/4a83ab41dfcf4880325159c2d5a5d3a3fb667eb0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Sofroniew
2. M. Pekny
3. B. Barres
4. C. Eroglu
5. N. J. Allen
6. J. Burda
7. M. Pekna
8. Kristen M. Harris

In Developmental Neuroscience

1. M. Sofroniew
2. M. Pekny
3. J. Burda
4. M. Pekna
5. B. Barres
6. C. Eroglu
7. N. J. Allen
8. H. Vinters

In Neurology

1. M. Sofroniew
2. B. Barres
3. M. Pekny
4. J. Burda
5. M. Pekna
6. N. J. Allen
7. C. Eroglu
8. H. Vinters

Citations in the corpus

• The Gabapentin Receptor α2δ-1 is the Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis (2009, positive): “Quantification of Synapse Numbers For synapse quantification of RGCs, we followed a previously developed immunohistochemistry (IHC)-based method described and validated in Christopherson et al. (2005) and Ullian et al.”
• The Aging Astrocyte Transcriptome from Multiple Regions of the Mouse Brain (2018, background): “We examined known synapse-inducing genes, thrombospondins (Thbs) and Sparcl1 (Hevin) (Christopherson et al., 2005; Kucukdereli et al., 2011), as well as astrocytic regulators of synaptic strength, Glypican 4 and 6 (Allen et al.”
• Purification and characterization of progenitor and mature human astrocytes reveals transcriptional and functional differences with mouse (2015, positive): “For example, purified neurons in culture have little ability to form functional synapses, which are powerfully promoted by astrocytes (Allen et al., 2012; Christopherson et al., 2005; Kucukdereli et al., 2011; Ullian et al., 2001).”
• Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “, by secreting vascular endothelial growth factor (VEGF), which stimulates formation of new blood vessels as well as synaptogenesis (20, 274), or by secretion of synaptogenic thrombospondin (45).”
• Balancing structure and function at hippocampal dendritic spines. (2008, background): “Astrocytes also secrete soluble factors such as thrombospondins and cholesterol, which influence spine formation and synapse maturation (Ullian et al. 2004, Christopherson et al. 2005).”
• STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury (2008, background): “Signaling regulation of astrocyte roles after SCI Astrocytes exert many activities essential to normal CNS function (Kettenmann and Ransom, 2004; Christopherson et al., 2005; Gensert and Ratan, 2006; Iadecola and Nedergaard, 2007; Pellerin et al., 2007).”
• Astrocytes and disease: a neurodevelopmental perspective. (2012, background): “The Barres laboratory (Christopherson et al. 2005; Eroglu et al. 2009) identified the proteins involved as TSPs, a group of matricellular proteins that are expressed in astrocytes of the developing but not mature brain, and TSP1/2deficient mice were shown to have reduced numbers of synapses in vivo.”
• The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential (2015, background): “However, thrombospondins promote formation of nonfunctional silent synapses (Christopherson et al., 2005), and thrombospondins destabilize postsynaptic a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid glutamate receptors (Hennekinne et al., 2013).”
• Reactive Astrocytes: Production, Function, and Therapeutic Potential. (2017, background): “As useful as these culture systems have been for the investigation of important astrocyte physiological functions (Christopherson et al., 2005; Eroglu et al., 2009; Allen et al., 2012), they are not representative of physiological astrocytes in vivo.”