ArticleFrontiers in endocrinology2021
Long Noncoding RNA X-Inactive-Specific Transcript Promotes the Secretion of Inflammatory Cytokines in LPS Stimulated Astrocyte Cell Via Sponging miR-29c-3p and Regulating Nuclear Factor of Activated T cell 5 Expression.
Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- lnc015013-CsMYB30-CsJAZ4/6 Module Co-Regulates JA Synthesis and Enhances Cold Hardiness in Tea Plants.International journal of molecular sciences · 2026Article
- miR-29c-3p downregulation accelerates spinal cord injury progression by targeting BRD4.Journal of orthopaedic surgery and research · 2025Article
- Article
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers.Frontiers in molecular neuroscience · 2025Review
- LncRNA XIST: A Breakthrough in Inflammation-related Diseases.Current medicinal chemistry · 2025Review
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Emerging roles of long non-coding RNAs in human epilepsy.Epilepsia · 2024Review
- Molecular mechanism analyses of post-traumatic epilepsy and hereditary epilepsy based on 10× single-cell transcriptome sequencing technology.CNS neuroscience & therapeutics · 2024Article
- Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- lncRNA XIST Interacts with Regulatory T Cells within the Tumor Microenvironment in Chronic Hepatitis B-Associated Hepatocellular Carcinoma.Turk patoloji dergisi · 2024Article
- Protective role of muscones on astrocytes under a mechanical-chemical damage model.Annals of translational medicine · 2022Article
- Erinacine A Prevents Lipopolysaccharide-Mediated Glial Cell Activation to Protect Dopaminergic Neurons against Inflammatory Factor-Induced Cell Death In Vitro and In Vivo.International journal of molecular sciences · 2022Article
- The lncRNAs at X Chromosome Inactivation Center: Not Just a Matter of Sex Dosage Compensation.International journal of molecular sciences · 2022Review
- Long non-coding RNAs: Potential therapeutic targets for epilepsy.Frontiers in neuroscience · 2022Review
- The role of noncoding RNAs in Parkinson's disease: biomarkers and associations with pathogenic pathways.Journal of biomedical science · 2021Review
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6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Astrocyte activation promotes glutamate accumulation and secretion of inflammatory factors, mainly responsible for epilepsy. Long noncoding RNA (lncRNA) X-inactive-specific transcript (XIST) regulates inflammation; however, the biological role and regulatory mechanism of XIST during astrocyte activation remain unclear. Methods: In the present study, rat epilepsy model and lipopolysaccharide (LPS)-treated CTX-TNA2 were established. XIST and miR-29c-3p expression were evaluated using quantitative real-time polymerase chain reaction. Nuclear factor of activated T cells 5 (NFAT5) was measured using western blot analysis. Interleukin (IL)-1β, IL-6, tumor necrosis factor-α, and L-glutamate levels in the culture supernatants were assessed using enzyme-linked immunosorbent assay. The binding between XIST and miR-29c-3p and between miR-29c-3p and the 3'-UTR of NFAT5 was analyzed using dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP), and Biotin pull-down assay. The proliferation and apoptosis were evaluated using CCK8 and flow cytometry, respectively. Results: XIST expression and NFAT5 protein level was increased, whereas miR-29c-3p expression was decreased in the epilepsy rat model and LPS-treated CTX-TNA2 cells. Silenced XIST expression, miR-29c-3p overexpression, or silenced NFAT5 expression inhibited the secretion of IL-1β, IL-6, and TNF-α and promoted glutamate transport in LPS-treated CTX-TNA2 cells. miR-29c-3p was the potential miRNA sponged by XIST. NFAT5 acted as a direct binding target of miR-29c-3p. Silenced miR-29c-3p expression or NFAT5 overexpression reversed the effect of silenced XIST expression on LPS-treated CTX-TNA2.XIST and miR-29c-3p treatment does not affect NFAT5 mRNA expression, but affects NFAT5 protein level. Furthermore, underexpressed XIST or overexpressed miR-29c-3p in LPS-stimulated CTX-TNA2 can attenuate neuronal apoptosis induced by LPS-stimulated CTX-TNA2. Conclusion: LncRNA XIST promotes the secretion of inflammatory cytokines in LPS- treated CTX-TNA2
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