Knockdown of Long Noncoding RNA H19 Represses the Progress of Pulmonary Fibrosis through the Transforming Growth Factor <i>β</i>/Smad3 Pathway by Regulating MicroRNA 140

Wang, Xi; Cheng, Zhe; Dai, Lingling; Jiang, Tianci; Jia, Liting; Jing, Xiaogang; An, L.; Wang, Huan; Li, Meng

doi:10.1128/mcb.00143-19

Cited by 52 publications

(40 citation statements)

References 33 publications

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“…Transforming growth factor-β1 (TGF-β1) was used to induce IPF of HPAEpiC cell model. [21][22][23] Cells were treated for 72 hours with 5 μg/mL TGF-β1 and 400 ng/mL vehicles, 5 μg/mL TGF-β1 and 10 μM bicyclol, negative control (NC) plasmid of miR-455-3p and 5 μg/mL TGF-β1, or miR-455-3p interference plasmid and 5 μg/mL TGF-β1, respectively. All plasmids obtained were purchased from GenePharma Co, Ltd (Shanghai, China).…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Zhou

Chai

2019

J of Cellular Biochemistry

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Idiopathic pulmonary fibrosis (IPF), a chronic, progressive and irreversible disease, needs long‐term treatment. Bicyclol was found to play a great role in pulmonary fibrosis, and the present study is to explore how bicyclol affects IPF with the involvement of microRNA‐455‐3p (miR‐455‐3p) and Bax. Bleomycin (BLM) was used to induce the IPF model in Sprague‐Dawley rats to detect the expression of miR‐455‐3p, Bax, and B‐cell lymphoma factor 2 (Bcl‐2). Moreover, to further investigate the mechanisms of bicyclol, the BLM‐induced fibrotic cell model was used after the lung epithelial cells HPAEpiC received miR‐455‐3p knockout treatment. The rats were then treated with vehicle and bicyclol, respectively. The apoptosis of fibrotic cells and Bax/Bcl‐2 were identified. Inhibition function of bicyclol was optimal at a dose of 150 mg/kg. Bicyclol inhibited cell apoptosis and reduced Bax/Bcl‐2 expression in rats. miR‐455‐3p could potentially bind to Bax gene. Bicyclol reduced the levels of methylenedioxyamphetamine, superoxide dismutase, and glutathione in rat lung tissue, inhibited the apoptosis of rats with IPF and upregulated miR‐455‐3p expression. In vitro studies showed that bicyclol significantly promoted miR‐455‐3p expression in HPAEpiC fibrosis. Bicyclol inhibited fibrosis‐induced apoptosis of HPAEpiC in alveolar epithelial cells through promoting miR‐455‐3p, which inhibited Bax expression in IPF. Bicyclol may suppress the apoptosis of alveolar epithelial cells by upregulating miR‐455‐3p. This study laid a theoretical foundation for further understanding of IPF and searching for new molecular therapeutic targets.

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Section: Cell Culture and Treatmentmentioning

confidence: 99%

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Zhou

Chai

2019

J of Cellular Biochemistry

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“…The current study indicated that H19 −/− mice attenuated the TGF-β/smad signaling in bleomycin damaged lungs by reducing the expression of Tgfb1 mRNA and activated the Smad2/3 protein. Consistently, in vitro study revealed that H19 can target miR-140 and regulate the TGF-β/Smad3 pathway [ 24 ]. Moreover, H19 could enhance TGF-β signaling in both hepatic stellate cells and hepatocytes and facilitate liver fibrosis [ 47 ].…”

Section: Discussionmentioning

confidence: 81%

“…The others and our recent studies both indicate that hepatic H19 level is correlated with the severity of cholestatic injury and liver fibrosis in mice [ 19 , 20 ]. Furthermore, H19 was also related to progression of lung cancer and lung fibrosis [ 21 – 24 ]. Although these studies suggest a causal link among H19 and pulmonary injury, it remains unknown whether and to what extent H19 is involved in the regulation of pulmonary fibrosis in vivo.…”

Section: Introductionmentioning

confidence: 99%

Long non-coding RNA H19 deficiency ameliorates bleomycin-induced pulmonary inflammation and fibrosis

Wang

Tian²,

Du³

et al. 2020

Respir Res

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Background The poor understanding of pathogenesis in idiopathic pulmonary fibrosis (IPF) impaired development of effective therapeutic strategies. The aim of the current study is to investigate the roles of long non-coding RNA H19 (lncRNA H19) in the pulmonary inflammation and fibrosis of IPF. Methods Bleomycin was used to induce pulmonary inflammation and fibrosis in mice. The mRNAs and proteins expression in lung tissues was determined by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. H19 knockout (H19−/−) mice were generated by CRISPR/Cas9. Results The expression of H19 mRNA was up-regulated in fibrotic lungs patients with IPF as well as in lungs tissues that obtained from bleomycin-treated mice. H19−/− mice suppressed bleomycin-mediated pulmonary inflammation and inhibited the Il6/Stat3 signaling. H19 deficiency ameliorated bleomycin-induced pulmonary fibrosis and repressed the activation of TGF-β/Smad and S1pr2/Sphk2 in the lungs of bleomycin-treated mice. Conclusions Our data suggests that H19 is a profibrotic lncRNA and a potential therapeutic target for IPF.

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“…A similar mechanism occurs between lncRNA NONMMUT065582 and miR-138, and lncRNA NON-MMUT022554 and miR-26a, during lung fibrosis [67,68]. The knock-down of lncRNA H19 diminishes lung pulmonary fibrosis by binding to miR-140, suggesting that H19 acts as sponge for miR-140 [69]. Meanwhile, H19 can play a molecular sponge role for miR-196a and miR-29b [70,71].…”

Section: The Role Of Circrna In the Development Of Ipfmentioning

confidence: 79%

Decrypting the crosstalk of noncoding RNAs in the progression of IPF

et al. 2020

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Idiopathic pulmonary fibrosis (IPF) is an agnogenic, rare, and lethal disease, with high mortality and poor prognosis and a median survival time as short as 3 to 5 years after diagnosis. No effective therapeutic drugs are still not available not only in clinical practice, but also in preclinical phases. To better and deeper understand pulmonary fibrosis will provide more effective strategies for therapy. Mounting evidence suggests that noncoding RNAs (ncRNAs) and their interactions may contribute to lung fibrosis; however, the mechanisms underlying their roles are largely unknown. In this review, we systematically summarized the recent advances regarding the crucial roles of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and circular RNAs (circRNAs) and crosstalk among them in the development of IPF. The perspective for related genes was well highlighted. In summary, ncRNA and their interactions play a key regulatory part in the progression of IPF and are bound to provide us with new diagnostic and therapeutic targets.

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Knockdown of Long Noncoding RNA H19 Represses the Progress of Pulmonary Fibrosis through the Transforming Growth Factor β/Smad3 Pathway by Regulating MicroRNA 140

Cited by 52 publications

References 33 publications

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Protective effect of bicyclol against pulmonary fibrosis via regulation of microRNA‐455‐3p in rats

Long non-coding RNA H19 deficiency ameliorates bleomycin-induced pulmonary inflammation and fibrosis

Decrypting the crosstalk of noncoding RNAs in the progression of IPF

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