CircRNA_0026344 via exosomal miR-21 regulation of Smad7 is involved in aberrant cross-talk of epithelium-fibroblasts during cigarette smoke-induced pulmonary fibrosis

Bai, Jun; Deng, Jianjun; Han, Zhixia; Cui, Yan; He, Renjiang; Gu, Yuanyun; Zhang, Qingbi

doi:10.1016/j.toxlet.2021.04.017

Cited by 29 publications

(15 citation statements)

References 42 publications

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“…Cigarette smoke is a major risk factor in IPF, which is widely used in IPF-related experiments such as myofibroblast differentiation, alveolar epithelial cell senescence, and mouse fibrosis model [ 33 , 34 , 35 ]. MLE-12 cells were exposed CSE for 24 h. In evaluating cellular proliferation, we performed Ki67 immunocytochemistry using MLE-12 cells treated with CSE or Lcar.…”

Section: Resultsmentioning

confidence: 99%

L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis

et al. 2022

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Idiopathic Pulmonary fibrosis (IPF), a chronic interstitial lung disease, has pulmonary manifestations clinically characterized by collagen deposition, epithelial cell injury, and a decline in lung function. L-carnosine, a dipeptide consisting of β-alanine and L-histidine, has demonstrated a therapeutic effect on various diseases because of its pivotal function. Despite the effect of L-carnosine in experimental IPF mice, its anti-oxidative effect and associated intercellular pathway, particularly alveolar epithelial cells, remain unknown. Therefore, we demonstrated the anti-fibrotic and anti-inflammatory effects of L-carnosine via Reactive oxygen species (ROS) regulation in bleomycin (BLM)-induced IPF mice. The mice were intratracheally injected with BLM (3 mg/kg) and L-carnosine (150 mg/kg) was orally administrated for 2 weeks. BLM exposure increased the protein level of Nox2, Nox4, p53, and Caspase-3, whereas L-carnosine treatment suppressed the protein level of Nox2, Nox4, p53, and Caspase-3 cleavage in mice. In addition, the total SOD activity and mRNA level of Sod2, catalase, and Nqo1 increased in mice treated with L-carnosine. At the cellular level, a human fibroblast (MRC-5) and mouse alveolar epithelial cell (MLE-12) were exposed to TGFβ1 following L-carnosine treatment to induce fibrogenesis. Moreover, MLE-12 cells were exposed to cigarette smoke extract (CSE). Consequently, L-carnosine treatment ameliorated fibrogenesis in fibroblasts and alveolar epithelial cells, and inflammation induced by ROS and CSE exposure was ameliorated. These results were associated with the inhibition of the NFκB pathway. Collectively, our data indicate that L-carnosine induces anti-inflammatory and anti-fibrotic effects on alveolar epithelial cells against the pathogenesis of IPF.

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Section: Resultsmentioning

confidence: 99%

L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis

et al. 2022

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“…For example, cir-cRNA_0026344 acts as a sponge for exosomal miR-21 to regulate Smad7 involved in aberrant crosstalk of epithelium-fibroblasts in the process of cigarette smoke-induced pulmonary fibrosis. 41 The lncRNA ZFAS1/miR-150-5p/SLC38A1 axis advances lung fibroblastto-myofibroblast transition and ferroptosis. 42 In present study, we constructed circRNA-mRNA, circRNA-miRNA, circRNA-miRNA-mRNA, lncRNA-mRNA, lncRNA-miRNA, lncRNA-miRNA-mRNA, and miRNA-mRNA networks.…”

Section: Discussionmentioning

confidence: 99%

“…The ceRNA network theory was widely applied in investigating the underlying mechanisms of many diseases. For example, circRNA_0026344 acts as a sponge for exosomal miR‐21 to regulate Smad7 involved in aberrant crosstalk of epithelium‐fibroblasts in the process of cigarette smoke‐induced pulmonary fibrosis 41 . The lncRNA ZFAS1 / miR‐150‐5p / SLC38A1 axis advances lung fibroblast‐to‐myofibroblast transition and ferroptosis 42 .…”

Section: Discussionmentioning

confidence: 99%

A transcriptomics‐based investigation of the mechanism of pulmonary fibrosis induced by nickel oxide nanoparticles

Liu,

Yang,

et al. 2024

Environmental Toxicology

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Nickel oxide nanoparticles (NiONPs) are an emerging nanomaterial, which poses a huge threat to the health of workplace population. Nanoparticles induce pulmonary fibrosis, and its mechanisms are associated with noncoding RNAs (ncRNAs). However, ncRNAs and competing endogenous RNA (ceRNA) networks which involved in NiONP‐induced pulmonary fibrosis are still unclear. This study aimed to identify ncRNA‐related ceRNA networks and investigate the role of the Wnt/β‐catenin pathway in pulmonary fibrosis. Male Wistar rats were intratracheally instilled with 0.015, 0.06, and 0.24 mg/kg NiONPs twice a week for 9 weeks. First, we found there were 93 circularRNAs (circRNAs), 74 microRNAs (miRNAs), 124 long non‐coding RNAs (lncRNAs), and 1675 messenger RNAs (mRNAs) differentially expressed through microarray analysis. Second, we constructed ceRNA networks among lncRNAs/circRNAs, miRNAs and mRNAs and identified two ceRNA networks (lncMelttl16/miR‐382‐5p/Hsd17b7 and circIqch/miR‐181d‐5p/Stat1) after real time‐quantitative polymerase chain reaction (RT–qPCR) validation. Furthermore, based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, ncRNAs were found to be involved in biological processes and signaling pathways related to pulmonary fibrosis. KEGG analysis showed that NiONPs activated the Wnt/β‐catenin pathway in rats. In vitro, HFL1 cells were treated with 0, 50, 100, and 200 μg/mL NiONPs for 24 h. We found that NiONPs induced collagen deposition and Wnt/β‐catenin pathway activation. Moreover, a blockade of Wnt/β‐catenin pathway alleviated NiONP‐induced collagen deposition. In conclusion, these observations suggested that ncRNAs were crucial in pulmonary fibrosis development and that the Wnt/β‐catenin pathway mediated the deposition of collagen.

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“…Pulmonary artery fibrosis was manifested as the elevation of vascular fibers and connective tissue and the decline of parenchymal cells, leading to the destruction of organ structure and vascular sclerosis. Multiple studies have elucidated that circRNA is involved in the progression of pulmonary fibrosis, covering circ0026344 [ 16 ], circ0000981 [ 17 ] and circ0044226 [ 18 ]. In this study, circRNA-SIRT1 was involved in the degree of pulmonary artery wall, which was supposed to have a critical association with pulmonary artery remodeling.…”

Section: Discussionmentioning

confidence: 99%

Circular RNA Sirtuin1 represses pulmonary artery smooth muscle cell proliferation, migration and autophagy to ameliorate pulmonary hypertension via targeting microRNA-145-5p/protein kinase-B3 axis

Jing

Liu

et al. 2022

Bioengineered

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Recently, several studies have been clarified that circular RNA (circRNA) was a vital regulatory gene of pulmonary hypertension (PH). Nevertheless, the action of circRNA in PH was not yet explored. This study was to figure out the biological function and potential molecular mechanism of circSirtuin1 (SIRT1) in PH. Construction of the PH rat model and hypoxia pulmonary artery smooth muscle cells (PASMC) model was performed, and test of circSIRT1/microRNA (miR)-145-5p/protein kinase-B3 (Akt3) was conducted. The influence of the circSIRT1/miR-145-5p/Akt3 axis on the histopathology, hemodynamics with autophagy of the pulmonary artery in rats was examined. Additionally, the impact of circSIRT1/miR-145-5p/Akt3 on the proliferation, migration and apoptosis with autophagy of PASMC under hypoxic environment was also determined. The targeting of circSIRT1/miR-145-5p/Akt3 was testified. The results manifested that circSIRT1 and Akt3 were elevated in PH, while miR-145-5p was declined. Knockdown of circSIRT1 ameliorated rat PH, suppressed PASMC proliferation, migration with autophagy in hypoxic environment. CircSIRT1 competitively combined with miR-145-5p to mediate Akt3. To sum up, circSIRT1/miR-145-5p/Akt3 was supposed to perform as a prospective molecular target for the treatment of PH.

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CircRNA_0026344 via exosomal miR-21 regulation of Smad7 is involved in aberrant cross-talk of epithelium-fibroblasts during cigarette smoke-induced pulmonary fibrosis

Cited by 29 publications

References 42 publications

L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis

L-carnosine Attenuates Bleomycin-Induced Oxidative Stress via NFκB Pathway in the Pathogenesis of Pulmonary Fibrosis

A transcriptomics‐based investigation of the mechanism of pulmonary fibrosis induced by nickel oxide nanoparticles

Circular RNA Sirtuin1 represses pulmonary artery smooth muscle cell proliferation, migration and autophagy to ameliorate pulmonary hypertension via targeting microRNA-145-5p/protein kinase-B3 axis

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