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

Wang, Xiaoyu; Tian, Xinbei; Du, Jun; Lu, Ying; Xiao, Yongtao

doi:10.1186/s12931-020-01534-6

Cited by 11 publications

(6 citation statements)

References 52 publications

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“…H19 downregulation alleviates fibroblast activation and lung fibrosis 77,78 . Wan et al 79 . further confirmed that H19 deficiency ameliorates bleomycin‐induced pulmonary infammation and fibrosis by using H19 knockout (H19−/−) mice generated by CRISPR/Cas9.…”

Section: Lncrna Directly Targets Non‐coding Genes To Regulate Pulmonary Fibrosismentioning

confidence: 91%

Long non‐coding RNAs: Promising new targets in pulmonary fibrosis

Zhang

Chen

Yue

et al. 2021

The Journal of Gene Medicine

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Pulmonary fibrosis is characterized by progressive and irreversible scarring in the lungs with poor prognosis and treatment. It is caused by various factors, including environmental and occupational exposures, and some rheumatic immune diseases. Even the rapid global spread of the COVID‐19 pandemic can also cause pulmonary fibrosis with a high probability. Functions attributed to long non‐coding RNAs (lncRNAs) make them highly attractive diagnostic and therapeutic targets in fibroproliferative diseases. Therefore, an understanding of the specific mechanisms by which lncRNAs regulate pulmonary fibrotic pathogenesis is urgently needed to identify new possibilities for therapy. In this review, we focus on the molecular mechanisms and implications of lncRNAs targeted protein‐coding and non‐coding genes during pulmonary fibrogenesis, and systematically analyze the communication of lncRNAs with various types of RNAs, including microRNA, circular RNA and mRNA. Finally, we propose the potential approach of lncRNA‐based diagnosis and therapy for pulmonary fibrosis. We hope that understanding these interactions between protein‐coding and non‐coding genes will contribute to the development of lncRNA‐based clinical applications for pulmonary fibrosis.

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Section: Lncrna Directly Targets Non‐coding Genes To Regulate Pulmonary Fibrosismentioning

confidence: 91%

Long non‐coding RNAs: Promising new targets in pulmonary fibrosis

Zhang

Chen

Yue

et al. 2021

The Journal of Gene Medicine

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“…The immunofluorescence assays were performed using the methods described previously. 13 , 22 Briefly, the liver sections were incubated with xylol and descending concentrations of ethanol. The endogenous peroxidases were removed by using 0.3% H 2 O 2 .…”

Section: Methodsmentioning

confidence: 99%

“…The western blots were performed as previously described. 22 , 23 Briefly, total protein lysates were extracted from the liver tissues or LX2 cells by using radioimmunoprecipitation buffer (Servicebio) supplemented with a protease inhibitor cocktail (Servicebio). The equal amounts of protein were separated on NuPAGE 10% Bis‐Tris gels (Invitrogen, Carlsbad, CA).…”

Section: Methodsmentioning

confidence: 99%

Upregulation of cadherin‐11 contributes to cholestatic liver fibrosis

Tian

Wang

et al. 2022

Pediatric Investigation

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Importance: , a cell-to-cell adhesion molecule, is implicated in the fibrotic process of several organs. Biliary atresia (BA) is a common cholestatic liver disease featuring cholestasis and progressive liver fibrosis in children. Cholestatic liver fibrosis may progress to liver cirrhosis and lacks effective therapeutic strategies. Currently, the role of CDH11 in cholestatic liver fibrosis remains unclear.Objective: This study aimed to explore the functions of CDH11 in cholestatic liver fibrosis. Methods: The expression of CDH11 in BA livers was evaluated by database analysis and immunostaining. Seven BA liver samples were used for immunostaining. The wild type (Wt) and CDH11 knockout (CDH11 -/-) mice were subjected to bile duct ligation (BDL) to induce cholestatic liver fibrosis. The serum biochemical analysis, liver histology, and western blotting were used to assess the extent of liver injury and fibrosis as well as activation of transforming growth factor-β (TGF-β)/Smad pathway. The effect of CDH11 on the activation of hepatic stellate cell line LX-2 cells was investigated. Results: Analysis of public RNA-seq datasets showed that CDH11 expression levels were significantly increased in livers of BA, and CDH11 was correlated with liver fibrosis in BA. BDL-induced liver injury and liver fibrosis were attenuated in CDH11 -/mice compared to Wt mice. The protein expression levels of phosphorylated Smad2/3 were decreased in livers of CDH11 -/-BDL mice compared to Wt BDL mice. CDH11 knockdown inhibited the activation of LX-2 cells. Interpretation: CDH11 plays an important role in cholestatic liver fibrosis and may represent a potential therapeutic target for cholestatic liver disease, such as BA.

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“…Pulmonary brosis was assessed from the lung histology. Lung histology was performed as described [15].…”

Section: Chemicals and Reagentsmentioning

confidence: 99%