ArticleJournal of neuroinflammation2016
Gas1 up-regulation is inducible and contributes to cell apoptosis in reactive astrocytes in the substantia nigra of LPS and MPTP models.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 24 citations in OpenAlex.
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- The mechanism of chronic intracellular infection withFrontiers in cellular and infection microbiology · 2023Review
- High-Frequency Repetitive Transcranial Magnetic Stimulation Regulates Astrocyte Activation by Modulating the Endocannabinoid System in Parkinson's Disease.Molecular neurobiology · 2022Article
- Caspase-dependent apoptosis induces reactivation and gliogenesis of astrocytes in adult mice.Frontiers in cellular neuroscience · 2022Article
- IGF-1 protects against angiotensin II-induced cardiac fibrosis by targeting αSMA.Cell death & disease · 2021Article
- Astrocyte Pannexin 1 Suppresses LPS-Induced Inflammatory Responses to Protect Neuronal SH-SY5Y Cells.Frontiers in cellular neuroscience · 2021Article
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- Sodium Butyrate and Indole-3-propionic Acid Prevent the Increase of Cytokines and Kynurenine Levels in LPS-induced Human Primary Astrocytes.International journal of tryptophan research : IJTR · 2020Article
- Treadmill Exercise Improves Motor Function by Suppressing Purkinje Cell Loss in Parkinson Disease Rats.International neurourology journal · 2018Article
- Glioprotective Effects of Lingonberry Extract Against Altered Cellular Viability, Acetylcholinesterase Activity, and Oxidative Stress in Lipopolysaccharide-Treated Astrocytes.Cellular and molecular neurobiology · 2018Article
- Neuroprotective effects of the gliopeptide ODN in an in vivo model of Parkinson's disease.Cellular and molecular life sciences : CMLS · 2018Article
- Expression of Gas1 in Mouse Brain: Release and Role in Neuronal Differentiation.Cellular and molecular neurobiology · 2018Article
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- Paeonol Protection Against Intrastriatal 6-Hydroxydopamine Rat Model of Parkinson's Disease.Basic and clinical neuroscienceArticle
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8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundReactive astrogliosis is a remarkable pathogenetic hallmark of the brains of Parkinson's disease (PD) patients, but its progressive fate and regulation mechanisms are poorly understood. In this study, growth arrest specific 1 (Gas1), a tumor growth suppressor oncogene, was identified as a novel modulator of the cell apoptosis of reactive astrocytes in primary culture and the injured substantia nigra.
methodsAnimal models and cell cultures were utilized in the present study. Lipopolysaccharide (LPS)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated animal models were used to detect Gas1 expression in the brain via immunohistochemistry and western blot. Cell cultures were performed to analyze Gas1 functions in the viability and apoptosis of reactive astrocytes and SH-SY5Y cells by double labeling, CCK-8, LDH, TUNEL, flow cytometry, and siRNA knockdown methods.
resultsGas1 expressions were significantly elevated in the majority of the reactive astrocytes of the brains with LPS or MPTP insults. In the injured substantia nigras, GFAP-positive astrocytes exhibited higher levels of cleaved caspase-3. In cell culture, the up-regulated Gas1 expression induced apoptosis of reactive astrocytes that were insulted by LPS in combination with interferon-γ and tumor necrosis factor-a. This effect was confirmed through siRNA knockdown of Gas1 gene expression. Finally and interestingly, the potential underlying signaling pathways were evidently related to an increase in the Bax/Bcl-2 ratio, the abundant generation of reactive oxygen species and the activation of cleaved caspase-3.
conclusionsThis study demonstrated that the up-regulation of inducible Gas1 contributed to the apoptosis of reactive astrocytes in the injured nigra. Gas1 signaling may function as a novel regulator of astrogliosis and is thus a potential intervention target for inflammatory events in PD conditions.
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