Circ-UQCRC2 aggravates lipopolysaccharide-induced injury in human bronchial epithelioid cells via targeting miR-495-3p/MYD88-mediated inflammatory response and oxidative stress

Zhang, Xuan; Chen, Chunbao; Li, Bei; Lu, Wei

doi:10.1080/08916934.2021.1975273

Cited by 8 publications

(10 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…also induced oxidative stress in bronchial epithelioid cells, and aggravated the inflammatory injury in infantile pneumonia. 21 CITED2 was repressed by hyperglycemia-induced oxidative stress in cultured embryos. CITED2 is essential for the homeostasis of endoplasmic reticulum stress and formation of neural tube defects during development of an embryo.…”

Section: Discussionmentioning

confidence: 95%

CITED2 alleviates lipopolysaccharide-induced inflammation and pyroptosis in - human lung fibroblast by inhibition of NF-κB pathway

Zhang

Chen

Liu

et al. 2022

Allergol Immunopathol

View full text Add to dashboard Cite

Background: Pneumonia, a severe infectious respiratory disease, is one of the leading causes of mortality and morbidity in children. Cbp/P300 interacting transactivator with Glu/Asp‑rich carboxyterminal domain 2 (CITED2) functions as a transcription cofactor, and plays critical roles in the development of embryonic and extra‑embryonic tissues, including fetal lung maturation. The present study investigates the role of CITED2 in infantile pneumonia. Methods: The human fetal lung fibroblasts (MRC‑5 and WI‑38) were treated with lipopolysac‑ charides to induce cytotoxicity, and the cell viability was detected by MTT. Inflammation was evaluated by ELISA, and western blot was used to investigate the pyroptosis. Results: CITED2 was down‑regulated in lipopolysaccharide‑treated MRC‑5/WI‑38 cells. The over‑expression of CITED2 protected MRC‑5 and WI‑38 cells from lipopolysaccharide‑ induced cytotoxicity by increasing the cell viability and decreasing LDH expression. CITED2 reduced the expression of TNF‑α, IL‑6, IL‑1β in lipopolysaccharide‑treated MRC‑5/WI‑38 cells. Lipopolysaccharide stimulated pyroptosis in MRC‑5 and WI‑38 cells through the up‑regulation of NL+RP3, GSDMD‑N, caspase‑1, IL‑1β and IL‑18. However, CITED2 down‑regulated the expression of NLRP3, GSDMD‑N, caspase‑1, IL‑1β, and IL‑18 protein in lipopolysaccharide‑treated MRC‑5/ WI‑38 cells. CITED2 also down‑regulated the protein expression of p‑p65 in lipopolysaccharide‑ treated MRC‑5/WI‑38 cells. Conclusion: CITED2 exhibited anti‑inflammatory effect on lipopolysaccharide‑treated human lung fibroblasts and reduced pyroptosis through inactivation of NF‑κB pathway.

show abstract

Section: Discussionmentioning

confidence: 95%

CITED2 alleviates lipopolysaccharide-induced inflammation and pyroptosis in - human lung fibroblast by inhibition of NF-κB pathway

Zhang

Chen

Liu

et al. 2022

Allergol Immunopathol

View full text Add to dashboard Cite

show abstract

“…As a matter of fact, circRNAs have aroused growing attention for the development of the ideal candidate biomarkers, based on their salient features, containing stability, conservation, abundance, and tissues and stage specificity (17,36). Lately, several circRNAs are being found to be frequently abnormally expressed in the pathological processes of pneumonia (37)(38)(39). Notably, LPS performs as a powerful proinflammatory molecule (40,41).…”

Section: Discussionmentioning

confidence: 99%

CIRCULAR RNA CIRC_0099188 CONTRIBUTES TO LPS-INDUCED HPAEpiC CELL INJURY BY TARGETING THE MIR-1236-3P/HMGB3 AXIS

Lin¹,

Zeng²,

Pan³

2023

Shock

View full text Add to dashboard Cite

Purpose: This study is designed to explore the role and mechanism of circ_0099188 in LPS-engendered HPAEpiC cells. Methods: Circ_0099188, microRNA-1236-3p (miR-1236-3p), and high mobility group box 3 (HMGB3) levels were measured using real-time quantitative polymerase chain reaction. Cell viability and apoptosis were assessed using cell counting kit-8 (CCK-8) and flow cytometry assays. Protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), cleaved-caspase 3, cleaved-caspase 9, and HMGB3 were determined using Western blot assay. IL-6, IL-8, IL-1β, and TNF-α levels were analyzed using enzyme-linked immunosorbent assays. After predicting using Circinteractome and Targetscan, the binding between miR-1236-3p and circ_0099188 or HMGB3 was verified using a dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Results: Circ_0099188 and HMGB3 were highly expressed, and miR-1236-3p was decreased in LPS-stimulated HPAEpiC cells. Also, the downregulation of circ_0099188 might overturn LPS-triggered HPAEpiC cell proliferation, apoptosis, and inflammatory response. Mechanically, circ_0099188 is able to affect HMGB3 expression by sponging miR-1236-3p. Conclusion: Circ_0099188 knockdown might mitigate LPS-induced HPAEpiC cell injury by targeting the miR-1236-3p/HMGB3 axis, providing an underlying therapeutic strategy for pneumonia treatment.

show abstract

“…MiRNAs are mostly endogenous RNAs and can regulate various physiological processes (13). Previous evidence has suggested that miRNAs have significant relevance to inflammation-related diseases, such as septic acute kidney injury (14), infantile pneumonia (15), and UC (16). MiRNAs can regulate immune cells, intestinal epithelial cell barrier, the homeostasis of intestinal microflora, and tumor formation in UC (16).…”

Section: Introductionmentioning

confidence: 99%

Circ_0085323 Silencing Inhibits TNF-Α-Induced Normal Human Colonic Epithelial Cell Inflammation and Apoptosis Through the Mir-495-3p/Traf3 Axis

An,

Yang,

Tao

et al. 2023

Shock

View full text Add to dashboard Cite

Background: Previous data have suggested the involvement of circular RNA (circRNA) in ulcerative colitis (UC) development. However, the role and mechanism of circ_0085323 in UC occurrence have not been reported. Methods: Normal human colonic epithelial cells (NCM460) were treated with TNF-α to simulate UC-like cell inflammation and injury in vitro. The expression of circ_0085323, microRNA-495-3p (miR-495-3p), and TNF receptor–associated factor 3 (TRAF3) was detected by quantitative real-time polymerase chain reaction. Protein expression was checked by western blotting analysis. Cell viability, cell proliferation, and cell apoptosis were investigated by cell counting kit-8 assay, 5-ethynyl-29-deoxyuridine assay, and flow cytometry analysis, respectively. IL-1β, IL-6, and IL-8 production were analyzed by enzyme-linked immunosorbent assays. Lactate dehydrogenase activity was assessed by a lactate dehydrogenase activity detection assay. The interactions among circ_0085323, miR-495-3p, and TRAF3 were identified by dual-luciferase reporter assay and RNA immunoprecipitation assay. Results: Circ_0085323 was overexpressed in the colonic mucosal tissues of UC patients and TNF-α–stimulated NCM460 cells. Circ_0085323 knockdown relieved TNF-α–induced inhibitory effect on the proliferation of NCM460 cells and promoting effects on cell apoptosis and inflammation. Circ_0085323 acted as a miR-495-3p sponge, and the effects of circ_0085323 silencing on TNF-α–induced NCM460 cell injury were attenuated by decreasing miR-495-3p expression. TRAF3 was targeted by miR-495-3p, and circ_0085323 combined with miR-495-3p to regulate TRAF3. TRAF3 depletion not only alleviated TNF-α–induced NCM460 cell damage but also partially revoked the effect of circ_0085323 silencing combined with miR-495-3p depletion on TNF-α–induced NCM460 cell injury. Conclusions: Circ_0085323 knockdown ameliorated TNF-α–induced NCM460 cell injury by regulating the miR-495-3p/TRAF3 axis, which suggested that circ_0085323 might be a therapeutic target for UC.

show abstract

Circ-UQCRC2 aggravates lipopolysaccharide-induced injury in human bronchial epithelioid cells via targeting miR-495-3p/MYD88-mediated inflammatory response and oxidative stress

Cited by 8 publications

References 36 publications

CITED2 alleviates lipopolysaccharide-induced inflammation and pyroptosis in - human lung fibroblast by inhibition of NF-κB pathway

CITED2 alleviates lipopolysaccharide-induced inflammation and pyroptosis in - human lung fibroblast by inhibition of NF-κB pathway

CIRCULAR RNA CIRC_0099188 CONTRIBUTES TO LPS-INDUCED HPAEpiC CELL INJURY BY TARGETING THE MIR-1236-3P/HMGB3 AXIS

Circ_0085323 Silencing Inhibits TNF-Α-Induced Normal Human Colonic Epithelial Cell Inflammation and Apoptosis Through the Mir-495-3p/Traf3 Axis

Contact Info

Product

Resources

About