miR‑1184 regulates inflammatory responses and cell apoptosis by targeting TRADD in an LPS‑induced cell model of sepsis

Ling, Ping; Tang, Rong; Wang, Huazhu; Deng, Xiuqin; Chen, Jianli

doi:10.3892/etm.2021.10062

Cited by 9 publications

(3 citation statements)

References 30 publications

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“…Wang and Han (30) showed that miR-1184 was decreased in the serum of neonatal sepsis, and overexpression of miR-1184 targetedly suppressed IL-6 level to inhibit LPS-stimulated inflammatory reaction in monocytes. Besides, miR-1184 exerted anti-inflammatory effects on LPS-induced in vitro sepsis cell model by suppressing TNF-R1-associated death domain protein (TRADD) expression (31). Consistent with these findings, we also found a decrease of miR-1184 level in sepsis patients and LPS-induced MRC-5 cells, and miR-1184 re-expression showed anti-apoptotic and anti-inflammatory action.…”

Section: Discussionmentioning

confidence: 99%

Circ_0033530 Knockdown Alleviates Lipopolysaccharide-Induced Acute Lung Injury Model of Human Lung Fibroblasts by Mir-1184/Tlr4 Axis

Xia,

Shan,

Luo

et al. 2023

Shock

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Background Circular RNAs (circRNAs) have been reported to be involved in regulating the progression of sepsis and sepsis-associated damage. Herein, this work investigated whether circ_0033530 had roles in the process of septic acute lung injury (sepsis-ALI) and its associated mechanism. Methods Lipopolysaccharide (LPS)-stimulated human lung fibroblasts MRC-5 were used to mimic the cell model of sepsis-ALI in vitro. Levels of genes and proteins were detected by qRT-PCR and western blotting. Functional experiments were conducted using 5-ethynyl-2’-deoxyuridine (EdU) assay, Cell counting Kit-8 (CCK-8) assay, flow cytometry, and Enzyme-Linked Immunosorbent Assay (ELISA), respectively. The interaction between miR-1184 and circ_0033530 or Toll-like receptor 4 (TLR4) was confirmed by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results Circ_0033530 expression was lower in sepsis patients and LSP-induced fibroblasts than those in healthy control and untreated cells. Functionally, knockdown of circ_0033530 protected fibroblasts against LPS-induced proliferation arrest, apoptosis and inflammatory response. Mechanistically, circ_0033530 acted as a sponge for miR-1184, and TLR4 RNA was targeted by miR-1184, indicating the circ_0033530/miR-1184/TLR4 axis. Further rescue experiments showed that circ_0033530 silencing-mediated growth inhibition and inflammation on fibroblasts were attenuated by miR-1184 down-regulation or TLR4 up-regulation. Conclusion Circ_0033530 knockdown alleviated LPS-induced proliferation arrest, apoptosis and inflammation in lung fibroblasts by miR-1184/TLR4 axis, provide molecular theoretical basis for circ_0033530 on the pathogenesis of sepsis-ALI.

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Section: Discussionmentioning

confidence: 99%

Circ_0033530 Knockdown Alleviates Lipopolysaccharide-Induced Acute Lung Injury Model of Human Lung Fibroblasts by Mir-1184/Tlr4 Axis

Xia,

Shan,

Luo

et al. 2023

Shock

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“…Once more, hsa-mir-449a inhibits cancer cell proliferation and promotes apoptosis which upturns the sensitivity to the chemotherapeutic drug resistance, so it has been considered as a therapeutic goal to alleviate chemotherapeutic drug resistance in cancer that will upsurge the effectiveness of chemotherapy [ 119 ]. hsa-mir-1184 has deregulated flow in the blood of children affected with Sepsis (Sepsis is a presumably harmful disease that happens when the body's immune system attacks its own tissues in response to an infection), along with that it can be an valuable recipient for the treatment of children with sepsis since it smears prohibited effects on inflammatory responses and apoptosis through assaulting TRADD (Tumor necrosis factor receptor type 1-associated DEATH domain protein) [ 120 ]. As well as hsa-mir-1976 has been termed as a non-invasive diagnostic object and therapeutic focus for sick sinus syndrome that is accompanying shortness of breath with opportunities to come across standpoints for mutually noticeable pathogenesis [ 121 ].…”

Section: Discussionmentioning

confidence: 99%

Systems biology models to identify the influence of SARS-CoV-2 infections to the progression of human autoimmune diseases

Al-Mustanjid

Mahmud

Akter

et al. 2022

Informatics in Medicine Unlocked

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“…For the experiments, cells in the logarithmic growth phase were utilized. THP-1 cells were treated with 1-µg/mL LPS for 24 h. 16 Following LPS treatment. A PSTPIP2 overexpression plasmid/vector was transfected into THP-1 cells using lipofectamine 3000 (Invitrogen, CA, USA).…”

Section: Thp-1 Cell Culture and Transfectionmentioning

confidence: 99%

PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects

Wang,

Luo

et al. 2023

Allergol Immunopathol

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Background: One of the common adverse reactions in patients with pressure ulcers (PU) is sepsis, which is mainly related to microbial infections caused by pathogenic organisms. The activation of nuclear factor kappa-B (NF-κB) frequently occurs in conjunction with pathogenic microbial infections. Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) is closely related to inflammatory disorders. The role and mechanism of PSTPIP2 in sepsis because of pressure ulcers is unclear. In this study, we discovered that PSTPIP2 was lowly expressed in peripheral blood of patients with sepsis induced by pressure ulcers. Methods: Peripheral blood was collected from 20 patients with sepsis due to pressure ulcers and 10 healthy controls, and the expression of PSTPIP2 in peripheral blood was discovered by polymerase chain reaction and Western blot analysis. Information on the clinical characteristics of patients was summarized, and the expression data of PSTPIP2 were correlated with the patients’ acute physiology and chronic health evaluation (APACHE) II score, sequential organ failure assessment (SOFA) score, and C-reactive protein (CRP) and procalcitonin (PCT) scores by Spearman’s correlation analysis. One of the main mediators of Gram-negative sepsis is lipopolysaccharide (LPS). In order to establish an in vitro sepsis model, THP-1 cells were treated with LPS, and the cells were transfected with PSTPIP2. Contents of interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor-α (TNF-α) in each group of cells were detected by enzyme-linked-immunosorbent serologic assay, and NF-κB-related proteins were detected by Western blot analysis. Results: When compared to healthy controls, the peripheral blood of patients with pressure sepsis had lower PSTPIP2 expression, which had a negative correlation with the APACHE II, SOFA, CRP, and PCT scores. LPS-induced THP-1 cells expressed less PSTPIP2 than the untreated control cells, and PSTPIP2 transfection decreased IL-6, IL-1β, and TNF-α levels and inhibited the activation of NF-κB pathway. Conclusion: PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects.

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miR‑1184 regulates inflammatory responses and cell apoptosis by targeting TRADD in an LPS‑induced cell model of sepsis

Cited by 9 publications

References 30 publications

Circ_0033530 Knockdown Alleviates Lipopolysaccharide-Induced Acute Lung Injury Model of Human Lung Fibroblasts by Mir-1184/Tlr4 Axis

Circ_0033530 Knockdown Alleviates Lipopolysaccharide-Induced Acute Lung Injury Model of Human Lung Fibroblasts by Mir-1184/Tlr4 Axis

Systems biology models to identify the influence of SARS-CoV-2 infections to the progression of human autoimmune diseases

PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects

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