Circular RNA circBbs9 promotes PM2.5-induced lung inflammation in mice via NLRP3 inflammasome activation

Li, Meizhen; Hua, Qiuhan; Shao, Yueting; Zeng, Huixian; Liu, Yuanyuan; Diao, Qinqin; Zhang, Han; Qiu, Miaoyun; Zhu, Jialu; Li, Xun; Ling, Yihui; Zhang, Rong; Jiang, Yiguo

doi:10.1016/j.envint.2020.105976

Cited by 81 publications

(28 citation statements)

References 41 publications

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“…An accumulated number of recent studies have identified that circRNAs are intensively associated with various respiratory diseases such as lung cancer, acute respiratory distress syndrome, pulmonary tuberculosis, pulmonary hypertension (PH), and silicosis ( Li et al, 2020 ; Lu et al, 2020 ; Wang L. et al, 2020 ; Zou et al, 2020 ). However, these studies focused exclusively on the functions of circRNAs in lung cancers and only a few have described their functions in other respiratory diseases.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0002062 Promotes the Proliferation of Pulmonary Artery Smooth Muscle Cells by Regulating the Hsa-miR-942-5p/CDK6 Signaling Pathway

Wang

Tan

et al. 2021

Front. Genet.

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Currently, new strategies for the diagnosis and treatment of hypoxia-induced pulmonary hypertension (HPH) are urgently required. The unique features of circRNAs have unveiled a novel perspective for understanding the biological mechanisms underlying HPH and the possibility for innovative strategies for treatment of HPH. CircRNAs function as competing endogenous RNAs (CeRNA) to sequester miRNAs and regulate the expression of target genes. This study aimed to explore the roles of hsa_circ_0002062 on the biological behaviors of pulmonary artery smooth muscle cells (PASMCs) in hypoxic conditions. A number of in vitro assays, such as RNA-binding protein immunoprecipitation (RIP), RNA pull-down, and dual-luciferase assays were performed to evaluate the interrelationship between hsa_circ_0002062, hsa-miR-942-5P, and CDK6. The potential physiological functions of hsa_circ_0002062, hsa-miR-942-5P, and CDK6 in hypoxic PASMCs were investigated through expression modulation. Our experiments demonstrated that hsa_circ_0002062 functions as a ceRNA, acts as a sponge for hsa-miR-942-5P, and consequently activates CDK6, which further promotes pulmonary vascular remodeling. Therefore, we speculate that hsa_circ_0002062 could serve as a candidate diagnostic biomarker and potential therapeutic target for HPH.

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Section: Discussionmentioning

confidence: 99%

Hsa_circ_0002062 Promotes the Proliferation of Pulmonary Artery Smooth Muscle Cells by Regulating the Hsa-miR-942-5p/CDK6 Signaling Pathway

Wang

Tan

et al. 2021

Front. Genet.

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“… 21 Lin et al exhibited that circHIPK3 contributed to proliferation and migration of airway smooth muscle cells in the development of asthma via the miR-326/STIM1 axis. 22 The researches of COPD have revealed that circBbs9 enhanced lung inflammation via targeting the miR-30e-5p/Adar pathway, 23 and hsa_circRNA_0008672 promoted the pathogenesis of COPD via acting on the miR-1265/MAPK1 axis. 24 …”

Section: Discussionmentioning

confidence: 99%

Circ-HACE1 Aggravates Cigarette Smoke Extract-Induced Injury in Human Bronchial Epithelial Cells via Regulating Toll-Like Receptor 4 by Sponging miR-485-3p

Zhou

Cao²,

Chai³

et al. 2021

COPD

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Background Smoking is the most common cause of chronic obstructive pulmonary disease (COPD), and the early diagnosis for COPD remains poor. Exploring the molecular mechanism and finding feasible biomarkers will be beneficial for clinical management of COPD. Circular RNAs (circRNAs) are noncoding RNAs that act as miRNA sponges to regulate the expression levels of genes, leading to the changes of cellular phenotypes and disease progression. CircRNA HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (circ-HACE1) was abnormally expressed after the induction of cigarette smoke extract (CSE) in cell model. This study was performed to explore its function and mechanism in COPD. Methods Circ-HACE1, microRNA-485-3p (miR-485-3p) and toll-like receptor 4 (TLR4) detection was performed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis/cell cycle were respectively examined using cell counting kit-8 (CCK-8) and flow cytometry. Inflammatory cytokines were determined by enzyme-linked immunosorbent assay (ELISA). Oxidative stress was evaluated through the measurement of malondialdehyde (MDA) and superoxide dismutase (SOD). The target binding analysis was conducted via dual-luciferase reporter assay. Western blot was employed for protein expression detection of TLR4. Results Circ-HACE1 was overexpressed in smokers or smokers with COPD and CSE upregulated circ-HACE1 expression in 16HBE cells. Knockdown of circ-HACE1 attenuated CSE-stimulated cell viability and cell cycle repression, as well as the enhancement of cell apoptosis, inflammatory response and oxidative stress. MiR-485-3p was a target of circ-HACE1. Circ-HACE1 regulated CSE-induced cell injury via targeting miR-485-3p. TLR4 was a downstream target of miR-485-3p, and miR-485-3p inhibited the CSE-induced cell damages by directly downregulating the level of TLR4. Circ-HACE1/miR-485-3p regulated TLR4 expression in CSE-treated 16HBE cells, and TLR4 overexpression also reversed all effects of si-circ-HACE1 on CSE-treated 16HBE cells. Conclusion These findings elucidated that circ-HACE1 contributed to the CSE-induced cell damages in COPD cell models via regulating TLR4 by acting as the sponge of miR-485-3p.

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“…Although it is not clear how circRNAs regulate the progression of in ammation, studies have shown that they may function as miRNA sponges to regulate the expression of target genes via the miRNA response element [31]. It has been reported that CircBbs9 can promote PM 2.5 -induced lung in ammation by activating NLRP3 via sponge miR-30e-5p [32]. In addition, circGLIS2 abnormally activates NF-κB signaling pathway through miR-671 sponge mechanism in colitis cells [33].…”

Section: Discussionmentioning

confidence: 99%

CircEpc1 Promotes Ricin Toxin-Induced Inflammation Via Activation of NF-κB And MAPK Signaling Pathways By Sponging miR-5114

Dong

Zhang

et al. 2021

Preprint

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Background: Increasing studies have concentrated on investigating circular RNAs (circRNAs) as pivotal regulators in the progression of numerous diseases and biological processes and abundant evidence shows that circRNAs are participated in the regulation of innate immune responses. Several studies showed that Ricin Toxin (RT) could induce inflammatory injury. There was no research on the particular functions and underlying mechanisms of circRNAs in RT-induced inflammation. Results: In this study, RNA sequencing performed on RT-treated and normal RAW264.7 macrophage cells was used to investigated the differentially expressed circRNAs. Based on the dataset, the expression of circEpc1 (mmu_circ_0000842) was identified higher in RT-treated cells. Moreover, gain-and-loss function assays showed that circEpc1 function as a promoter in RT-induced inflammation in vivo and in vitro. Mechanistically, circEpc1 acted as a miR-5114 sponge to relieve the suppressive effect of miR-5114 on its target NOD2 and thereby activating NF-κB and MAPK signaling pathways. Conclusions: Our results illuminated a link between RT-induced inflammation and the circEpc1 regulatory loop and provided novel insight into the functions of circRNA in innate immune, which may emerge as a potential target in immunotherapy to control the RT-induced inflammatory injury.

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Circular RNA circBbs9 promotes PM2.5-induced lung inflammation in mice via NLRP3 inflammasome activation

Cited by 81 publications

References 41 publications

Hsa_circ_0002062 Promotes the Proliferation of Pulmonary Artery Smooth Muscle Cells by Regulating the Hsa-miR-942-5p/CDK6 Signaling Pathway

Hsa_circ_0002062 Promotes the Proliferation of Pulmonary Artery Smooth Muscle Cells by Regulating the Hsa-miR-942-5p/CDK6 Signaling Pathway

Circ-HACE1 Aggravates Cigarette Smoke Extract-Induced Injury in Human Bronchial Epithelial Cells via Regulating Toll-Like Receptor 4 by Sponging miR-485-3p

CircEpc1 Promotes Ricin Toxin-Induced Inflammation Via Activation of NF-κB And MAPK Signaling Pathways By Sponging miR-5114

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