ArticleJournal of inflammation (London, England)2022
CircRNA circFADS2 is under-expressed in sepsis and protects lung cells from LPS-induced apoptosis by downregulating miR-133a.
Article in Journal of inflammation (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Hsa_circ_0000313/miR-1224-3p/MKNK2 Axis Modulates CD4Mediators of inflammation · 2026Article
- Transcriptome sequencing showed the differential expression of circRNAs in human pulmonary microvascular endothelial cells in acute respiratory distress syndrome.Journal of thoracic disease · 2025Article
- Exosomes as novel biomarkers in sepsis and sepsis related organ failure.Journal of translational medicine · 2024Review
- CircMAPK1 induces cell pyroptosis in sepsis-induced lung injury by mediating KDM2B mRNA decay to epigenetically regulate WNK1.Molecular medicine (Cambridge, Mass.) · 2024Article
- Circular RNAs as potential biomarkers for male severe sepsis.Open life sciences · 2024Article
- N6-methyladenosine methylation analysis of circRNAs in acquired middle ear cholesteatoma.Frontiers in genetics · 2024Article
- Obesity-induced inflammatory miR-133a mediates apoptosis of granulosa cells and causes abnormal folliculogenesis.Acta biochimica et biophysica Sinica · 2023Article
- The Intricate Role of Non-Coding RNAs in Sepsis-Associated Disseminated Intravascular Coagulation.International journal of molecular sciences · 2023Review
- Circular RNA protein tyrosine kinase 2 aggravates pyroptosis and inflammation in septic lung tissue by promoting microRNA-766/eukaryotic initiation factor 5A axis-mediated ATP efflux.Acta cirurgica brasileira · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
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Abstract
backgroundIt has been reported that hsa_circRNA_100833 (identified as circFADS2) and miR-133a play opposite roles in LPS-induced cell apoptosis, which contributes to the development of sepsis. This study was carried out to explore the interaction between circFADS2 and miR-133a in sepsis.
methodsExpression of circFADS2 and miR-133a in plasma from both sepsis patients (n=62) and healthy controls (n=62) was studied by RT-qPCR. Pearson's correlation coefficient analysis was utilized to analyze the correlation between circFADS2 and miR-133a levels across plasma samples from sepsis patients. Cell viability and apoptosis, levels of proteins associated with apoptosis (cleaved caspase-3 and cleaved caspase-9), and expression of pro-inflammatory cytokines in LPS-treated HBEpCs were detected by MTT assay, cell apoptosis assay, western blot, and ELISA, respectively. In addition, a dual-luciferase reporter assay was performed to verify the interaction between circFADS2 and miR-133a.
resultsCircFADS2 was under-expressed (0.56-fold vs. control) in sepsis, and miR-133a was highly expressed (2.05-fold vs. control) in sepsis. An inverse correlation between circFADS2 and miR-133a was observed across sepsis samples. LPS decreased cell viability, increased cell apoptosis, and elevated productions of tumor necrosis factor (TNF)-α, interleukins (IL)-1β, IL-6, and IL-8 in HBEpCs in a dose-dependent manner. In addition, circFADS2 was identified as a target gene of miR-133a. The further experiment revealed that circFADS2 overexpression and miR-133a inhibition prominently promoted cell viability (1.71-fold vs. pcDNA3.1; 1.65-fold vs. NC miRNA) and decreased apoptosis of LPS-treated HBEpCs (0.44-fold vs. pcDNA3.1; 0.47-fold vs. NC miRNA). Moreover, circFADS2 knockdown and miR-133a overexpression inhibited viability (0.36-fold vs. pcDNA3.1; 0.37-fold vs. NC miRNA) and increased apoptosis (1.54-fold vs. pcDNA3.1; 1.51-fold vs. NC miRNA) of LPS-treated HBEpCs. Notably, circFADS2 overexpression reduced the effects of miR-133a on LPS-treated HBEpCs.
conclusionsCircFADS2 is under-expressed in sepsis and may protect lung cells from LPS-induced apoptosis by downregulating miR-133a.
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