ArticleCurrent pharmaceutical design2023
LncRNA GAS5 as an Inflammatory Regulator Acting through Pathway in Human Lupus.
Article in Current pharmaceutical design, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Serum from Antiphospholipid Syndrome Patients Downregulates Endothelial lncRNAs HIF1A-AS1 and OIP5-AS1.International journal of molecular sciences · 2026Article
- Decoding the lncRNA World: Comprehensive Approaches to lncRNA Structure and Interactome Studies.Cells · 2026Review
- The long non-coding RNA GAS5 contributes to the suppression of inflammatory responses by inhibiting NF-κB activity.Frontiers in pharmacology · 2024Article
- An updated review on abnormal epigenetic modifications in the pathogenesis of systemic lupus erythematosus.Frontiers in immunology · 2024Review
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
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Abstract
aimTo investigate the contribution of GAS5 in the pathogenesis of SLE.
backgroundSystemic Lupus Erythematosus (SLE) is characterized by aberrant activity of the immune system, leading to variable clinical symptoms. The etiology of SLE is multifactor, and growing evidence has shown that long noncoding RNAs (lncRNAs) are related to human SLE. Recently, lncRNA growth arrest-specific transcript 5 (GAS5) has been reported to be associated with SLE. However, the mechanism between GAS5 and SLE is still unknown.
objectiveFind the specific mechanism of action of lncRNA GAS5 in SLE.
methodsCollecting samples of the SLE patients, Cell culture and treatment, Plasmid construction, and transfection, Quantitative real-time PCR analysis, Enzyme-linked immunosorbent assay (ELISA), Cell viability analysis, Cell apoptosis analysis, Western blot.
resultsIn this research, we investigated the contribution of GAS5 in the pathogenesis of SLE. We confirmed that, compared to healthy people, the expression of GAS5 was significantly decreased in peripheral monocytes of SLE patients. Subsequently, we found that GAS5 can inhibit the proliferation and promote the apoptosis of monocytes by over-expressing or knocking down the expression of GAS5. Additionally, the expression of GAS5 was suppressed by LPS. Silencing GAS5 significantly increased the expression of a group of chemokines and cytokines, including IL-1β, IL-6, and THFα, which were induced by LPS. Furthermore, it was identified the involvement of GAS5 in the TLR4-mediated inflammatory process was through affecting the activation of the MAPK signaling pathway.
conclusionIn general, the decreased GAS5 expression may be a potential contributor to the elevated production of a great number of cytokines and chemokines in SLE patients. And our research suggests that GAS5 contributes a regulatory role in the pathogenesis of SLE, and may provide a potential target for therapeutic intervention.
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