ArticleJournal of molecular neuroscience : MN2015
The regulation of Sox2 and Sox9 stimulated by ATP in spinal cord astrocytes.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- SOX Genes in Spinal Cord Injury: Redefining Neural Stem Cell Regeneration Strategies.Molecular neurobiology · 2025Review
- The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes.Biomedicines · 2024Article
- Modulating neuroinflammation through molecular, cellular and biomaterial-based approaches to treat spinal cord injury.Bioengineering & translational medicine · 2023Review
- Astrocytes in Post-traumatic Stress Disorder.Neuroscience bulletin · 2022Review
- Astrocyte phenotypes: Emphasis on potential markers in neuroinflammation.Histology and histopathology · 2021Review
- Extracellular ATP promotes breast cancer invasion and chemoresistance via SOX9 signaling.Oncogene · 2020Article
- Purinergic signaling in the retina: From development to disease.Brain research bulletin · 2019Review
- Curcumin Can Improve Spinal Cord Injury by Inhibiting TGF-β-SOX9 Signaling Pathway.Cellular and molecular neurobiology · 2019Review
- Microenvironment Imbalance of Spinal Cord Injury.Cell transplantation · 2018Review
- Effect of CLIP3 Upregulation on Astrocyte Proliferation and Subsequent Glial Scar Formation in the Rat Spinal Cord via STAT3 Pathway After Injury.Journal of molecular neuroscience : MN · 2018Article
- Primary Cell Culture of Live Neurosurgically Resected Aged Adult Human Brain Cells and Single Cell Transcriptomics.Cell reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After spinal cord injury (SCI), the level of adenosine triphosphate (ATP) and extracellular matrix (ECM) is increased. Formation of the glial scar is a complex process that is primarily attributed to astrocytic proliferation, and the fibrotic scar results from ECM deposition. In our previous researches, ATP and fibronectin was able to separately stimulate the proliferation of astrocytes. Moreover, fibronectin increases the expression of P2Y1 receptor and offers more binding sites for ATP, which aggravates the proliferation. Meanwhile, ATP was also able to stimulate the release of interleukin (IL)-6 and tumor necrosis factor-α (TNF-α), but fibronectin does not. Recently, it has been reported that over-expressing P2Y1 receptor could promote the level of Sox9. However, the regulation of Sox genes by ATP is still little known in spinal cord astrocytes. In the present study, we discovered that ATP was able to increase the expression of Sox2 and Sox9; fibronectin did not have this direct function. Sox9 was only involved in the proliferation increased by ATP, and Sox2 influenced the release of IL-6 stimulated by ATP. Understanding the critical role of Sox2 and Sox9 mediated by ATP may provide a potential target for therapeutic intervention in spinal cord injury.
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