LncRNA Gm16410 regulates PM2.5-induced lung Endothelial-Mesenchymal Transition via the TGF-β1/Smad3/p-Smad3 pathway

Ma, Kexin; Li, Cailong; Xu, Jingbin; Ren, Fei; Xu, Xin; Liu, Chaosheng; Niu, Ben; Li, Fasheng

doi:10.1016/j.ecoenv.2020.111327

Cited by 24 publications

(12 citation statements)

References 27 publications

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“…The conversion of endothelial cells into fibroblasts during the EndMT was originally described in the context of experimental wound repair [27]. Endothelial cells have also been reported to contribute to fibroblast production and aggregation in fibrotic diseases of the lung, heart, eye, kidney and other organs [28][29][30][31]. The EndMT is characterised by the loss of intercellular junctions between endothelial cells, which acquire an invasive and migratory phenotype and exhibit upregulated expression of mesenchymal cell markers such as alpha-smooth muscle actin (α-SMA), fibroblast-specific protein-1 and vimentin.…”

Section: Introductionmentioning

confidence: 99%

EndMT: New findings on the origin of myofibroblasts in endometrial fibrosis of intrauterine adhesions

Bao

Fan

et al. 2022

Reprod Biol Endocrinol

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Background Intrauterine adhesion (IUA) is one of the leading causes of infertility and the main clinical challenge is the high recurrence rate. The key to solving this dilemma lies in elucidating the mechanisms of endometrial fibrosis. The aim of our team is to study the mechanism underlying intrauterine adhesion fibrosis and the origin of fibroblasts in the repair of endometrial fibrosis. Methods Our experimental study involving an animal model of intrauterine adhesion and detection of fibrosis-related molecules. The levels of molecular factors related to the endothelial-to-mesenchymal transition (EndMT) were examined in a rat model of intrauterine adhesion using immunofluorescence, immunohistochemistry, qPCR and Western blot analyses. Main outcome measures are levels of the endothelial marker CD31 and the mesenchymal markers alpha-smooth muscle actin (α-SMA) and vimentin. Results Immunofluorescence co-localization of CD31 and a-SMA showed that 14 days after moulding, double positive cells for CD31 and a-SMA could be clearly observed in the endometrium. Decreased CD31 levels and increased α-SMA and vimentin levels indicate that EndMT is involved in intrauterine adhesion fibrosis. Conclusions Endothelial cells promote the emergence of fibroblasts via the EndMT during the endometrial fibrosis of intrauterine adhesions.

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Section: Introductionmentioning

confidence: 99%

EndMT: New findings on the origin of myofibroblasts in endometrial fibrosis of intrauterine adhesions

Bao

Fan

et al. 2022

Reprod Biol Endocrinol

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“…Recently, a lncRNA microarray analysis revealed that 201 lncRNAs are upregulated and 108 lncRNAs are downregulated in the lung tissue of Balb/c mice exposed to PM 2.5 . The mechanism of EndMT and the upregulated lncRNA Gm16410 was further investigated and it was found that lncRNA Gm16410 mediates PM2.5‐induced EndMT by regulating the TGF‐β1/Smad3/p‐Smad3 pathway, which highlights the potential of lncRNAs to promote pulmonary fibrosis under environmental pollution 57 …”

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

confidence: 98%

“…pathway, which highlights the potential of lncRNAs to promote pulmonary fibrosis under environmental pollution. 57 The above-mentioned lncRNAs, located in various cells that directly target protein-coding genes to regulate pulmonary fibrosis, are listed in Table 1.…”

Section: Lncrna In Macrophagesmentioning

confidence: 99%

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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“…PM2.5 have been reported in EMT transition which contributes in lung brosis. Among these upregulated lncRNA, it was discovered that Gm16410 regulates the TGF-β1/Smad3/p-Smad3 signaling pathway [94].…”

Section: Lncrnamentioning

confidence: 99%

Non-Coding RNA in Idiopathic Interstitial Pneumonia and Covid-19 Pulmonary Fibrosis

Ali

Singh

Alam

et al. 2022

Preprint

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Pulmonary fibrosis is the major manifestation of idiopathic interstitial pneumonia as well as post-COVID-19 complications. The pathogenesis of PF is a complex molecular process that involves many types of cells, proteins, genes, and regulatory elements. The non-coding RNA is the main regulatory element in this process which mainly includes; miRNA, circRNA, and lncRNA. These regulatory elements control the expression of many important genes and various pathways that are involved in the pathogenesis of pulmonary fibrosis. Identification and molecular mechanisms by which these non-coding RNA molecules works are very important because they do not only help to understand the molecular basis of the disease but could also serve as a potential diagnostic/prognostic marker as well as therapeutic targets. In this review, we have provided the latest findings and discussed the role of these regulatory elements in various biological processes and pathways involved in the pathogenesis of pulmonary fibrosis associated with IIPs and Covid-19.

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LncRNA Gm16410 regulates PM2.5-induced lung Endothelial-Mesenchymal Transition via the TGF-β1/Smad3/p-Smad3 pathway

Cited by 24 publications

References 27 publications

EndMT: New findings on the origin of myofibroblasts in endometrial fibrosis of intrauterine adhesions

EndMT: New findings on the origin of myofibroblasts in endometrial fibrosis of intrauterine adhesions

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

Non-Coding RNA in Idiopathic Interstitial Pneumonia and Covid-19 Pulmonary Fibrosis

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