Regulatory network of two circRNAs and an miRNA with their targeted genes under astilbin treatment in pulmonary fibrosis

Lu, Guangping; Zhang, Jinjin; Liu, Xiangyong; Liu, Wenbo; Cao, Guohong; Lv, Changjun; Zhang, Xiaoli; Xu, Pan; Li, Minge; Song, Xiaodong

doi:10.1111/jcmm.14550

Cited by 21 publications

(15 citation statements)

References 50 publications

(100 reference statements)

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“…However, little is known about these functions in pulmonary fibrosis. Only one study has addressed that miR‐29b‐2‐5p is down‐regulated in bleomycin‐induced fibrotic murine lung tissues and seems to participate in TGF‐β1‐induced lung fibroblast activation 23 . Another study reported that the expression of miR‐34c‐3p was reduced in the lung tissues of rats and A549 cells exposed to silica 24 .…”

Section: Discussionmentioning

confidence: 99%

LncRNA‐ATB regulates epithelial‐mesenchymal transition progression in pulmonary fibrosis via sponging miR‐29b‐2‐5p and miR‐34c‐3p

Cheng

Liu

et al. 2021

J Cellular Molecular Medi

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Dysregulation of non‐coding RNAs (ncRNAs) has been proved to play pivotal roles in epithelial‐mesenchymal transition (EMT) and fibrosis. We have previously demonstrated the crucial function of long non‐coding RNA (lncRNA) ATB in silica‐induced pulmonary fibrosis‐related EMT progression. However, the underlying molecular mechanism has not been fully elucidated. Here, we verified miR‐29b‐2‐5p and miR‐34c‐3p as two vital downstream targets of lncRNA‐ATB. As opposed to lncRNA‐ATB, a significant reduction of both miR‐29b‐2‐5p and miR‐34c‐3p was observed in lung epithelial cells treated with TGF‐β1 and a murine silicosis model. Overexpression miR‐29b‐2‐5p or miR‐34c‐3p inhibited EMT process and abrogated the pro‐fibrotic effects of lncRNA‐ATB in vitro. Further, the ectopic expression of miR‐29b‐2‐5p and miR‐34c‐3p with chemotherapy attenuated silica‐induced pulmonary fibrosis in vivo. Mechanistically, TGF‐β1‐induced lncRNA‐ATB accelerated EMT as a sponge of miR‐29b‐2‐5p and miR‐34c‐3p and shared miRNA response elements with MEKK2 and NOTCH2, thus relieving these two molecules from miRNA‐mediated translational repression. Interestingly, the co‐transfection of miR‐29b‐2‐5p and miR‐34c‐3p showed a synergistic suppression effect on EMT in vitro. Furthermore, the co‐expression of these two miRNAs by using adeno‐associated virus (AAV) better alleviated silica‐induced fibrogenesis than single miRNA. Approaches aiming at lncRNA‐ATB and its downstream effectors may represent new effective therapeutic strategies in pulmonary fibrosis.

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Section: Discussionmentioning

confidence: 99%

LncRNA‐ATB regulates epithelial‐mesenchymal transition progression in pulmonary fibrosis via sponging miR‐29b‐2‐5p and miR‐34c‐3p

Cheng

Liu

et al. 2021

J Cellular Molecular Medi

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“…with limited ability to encode proteins and usually form a closed circular structure covalently joined by the 3′ and 5′ ends. 8,9 Accumulating evidences about circRNAs have demonstrated that they can impact diverse biological processes and are also implicated in tumour generation and development. [10][11][12] The most investigated function of cir-cRNAs is as master regulators of gene expression that act to sequester or 'sponge' other gene expression regulators, such as miRNAs.…”

Section: Circular Rnas (Circrnas) Are a Class Of Non-coding Rnas (Ncrmentioning

confidence: 99%

“…Circular RNAs (circRNAs) are a class of non‐coding RNAs (ncRNAs) with limited ability to encode proteins and usually form a closed circular structure covalently joined by the 3′ and 5′ ends 8,9 . Accumulating evidences about circRNAs have demonstrated that they can impact diverse biological processes and are also implicated in tumour generation and development 10‐12 .…”

Section: Introductionmentioning

confidence: 99%

Circular RNA hsa_circ_0000658 inhibits osteosarcoma cell proliferation and migration via the miR‐1227/IRF2axis

Jiang

Chen

2020

J Cellular Molecular Medi

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Osteosarcoma (OS) is the most common type of primary bone cancer with malignancy, and it arises from malignant mesenchymal cells producing immature bone and/or osteoid. 1,2 Moreover, it ranks second in regard to the cause of death associated with cancer in children and teenagers. 3 Recently, patients with OS exhibiting no distant metastasis have been shown to project a 5-year survival rate of approximately 65%-70%, which could be attributed to surgery combined with chemotherapy, a major strategy implemented for treating OS. 4 However, this rate in patients exhibiting pulmonary metastasis at an early stage is only 20%, in spite of the advances in chemotherapeutics and surgical techniques, as OS exhibits high-grade malignancy, resistance to chemotherapies and aggressive behaviour. 5-7 Over the last two or three decades, only slight progress has been made in establishing robust treatment

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“…In a mouse model of concanavalin A (Con A)-induced hepatitis, administration of astilbin leads to improvement of the T cell-mediated liver injury by suppression of transaminase activity and TNF-α production [8]. Recently, circular RNAs (cir-cRNAs) profiling analysis showed that a total of 145 cir-cRNAs were differentially expressed in the astilbin-treat-ed rats exposed to bleomycin, suggesting the transcriptome complexity at the circRNA level under astilbin treatment [13]. Consistently, this study demonstrated that astilbin dose-dependently ameliorated pathological lesions, collagen accumulation, and hydroxyproline content.…”

Section: Discussionmentioning

confidence: 99%

Astilbin Protects Against Carbon Tetrachloride-Induced Liver Fibrosis in Rats

Sun¹,

Zhang²,

Fan³

et al. 2021

Pharmacology

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Background: Hepatic fibrosis is an inflammatory liver disease, and there is no effective therapy at present. Astilbin is a bioactive ingredient found in many medicinal and food plants, with antioxidative, anti-inflammatory, and antitumor properties. Objectives: This study aimed to investigate the protective effect and related molecular mechanism of astilbin against carbon tetrachloride (CCl4)-induced liver fibrosis in rats. Methods: Liver fibrosis was induced by injection of CCl4 in male Sprague-Dawley rats, and those rats were then treated with astilbin at different concentrations. Pathological changes, collagen production, inflammatory cytokine, and oxidative stress were evaluated to evaluate the effects of astilbin on CCl4-induced hepatic fibrosis. Real-time PCR and western blot were performed to detect the mRNA and protein expression of indicated genes. Results: We discovered that CCl4 caused significant fibrosis damage in rat liver, and astilbin dose-dependently improved the liver functions and fibrosis degree. Astilbin treatment significantly decreased collagen production, inflammatory response, and oxidative stress in vivo. Mechanically, administration of astilbin obviously elevated the hepatic levels of Nrf2 and its downstream components, including NAD(P)H:quinone oxidoreductase 1 (Nqo1), heme oxygenase (HO-1), glutamate-cysteine ligase catalytic subunit, and glutamate cysteine ligase modifier. Conclusions: Taken together, these findings demonstrate that astilbin could protect against CCL4 induced-liver fibrosis in rats.

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Regulatory network of two circRNAs and an miRNA with their targeted genes under astilbin treatment in pulmonary fibrosis

Cited by 21 publications

References 50 publications

LncRNA‐ATB regulates epithelial‐mesenchymal transition progression in pulmonary fibrosis via sponging miR‐29b‐2‐5p and miR‐34c‐3p

LncRNA‐ATB regulates epithelial‐mesenchymal transition progression in pulmonary fibrosis via sponging miR‐29b‐2‐5p and miR‐34c‐3p

Circular RNA hsa_circ_0000658 inhibits osteosarcoma cell proliferation and migration via the miR‐1227/IRF2axis

Astilbin Protects Against Carbon Tetrachloride-Induced Liver Fibrosis in Rats

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