LncRNA H19-mediated M2 polarization of macrophages promotes myofibroblast differentiation in pulmonary fibrosis induced by arsenic exposure

Xiao, Tian; Zou, Zhonglan; Xue, Junchao; Syed, Binafsha Manzoor; Sun, Jing; Dai, Xiangyu; Shi, Ming; Li, Junjie; Wei, Shaofeng; Tang, Huanwen; Zhang, Aihua; Liu, Qizhan

doi:10.1016/j.envpol.2020.115810

Cited by 58 publications

(41 citation statements)

References 51 publications

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“…NRAS encodes GTPases involved in cell growth, proliferation and differentiation, and its protein products lead to downstream signaling events [ 35 , 36 ]. MYC may promote the exacerbation of pulmonary fibrosis according to immune regulation [ 37 , 38 ], and be a key gene according to the interaction network. MYC produces c-myc proto-oncoprotein, which acts down-stream of multiple growth factor signaling pathways, and MYC amplification was significantly associated with squamous cell lung carcinoma (SCC) in IPF patients [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

An 8-ferroptosis-related genes signature from Bronchoalveolar Lavage Fluid for prognosis in patients with idiopathic pulmonary fibrosis

Shang²,

et al. 2022

BMC Pulm Med

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Background With the rapid advances of genetic and genomic technologies, the pathophysiological mechanisms of idiopathic pulmonary fibrosis (IPF) were gradually becoming clear, however, the prognosis of IPF was still poor. This study aimed to systematically explore the ferroptosis-related genes model associated with prognosis in IPF patients. Methods Datasets were collected from the Gene Expression Omnibus (GEO). The least absolute shrinkage and selection operator (LASSO) Cox regression analysis was applied to create a multi-gene predicted model from patients with IPF in the Freiburg cohort of the GSE70866 dataset. The Siena cohort and the Leuven cohort were used for validation. Results Nineteen differentially expressed genes (DEGs) between the patients with IPF and control were associated with poor prognosis based on the univariate Cox regression analysis (all P < 0.05). According to the median value of the risk score derived from an 8-ferroptosis-related genes signature, the three cohorts’ patients were stratified into two risk groups. Prognosis of high-risk group (high risk score) was significantly poorer compared with low-risk group in the three cohorts. According to multivariate Cox regression analyses, the risk score was an independently predictor for poor prognosis in the three cohorts. Receiver operating characteristic (ROC) curve analysis and decision curve analysis (DCA) confirmed the signature's predictive value in the three cohorts. According to functional analysis, inflammation- and immune-related pathways and biological process could participate in the progression of IPF. Conclusions These results imply that the 8-ferroptosis-related genes signature in the bronchoalveolar lavage samples might be an effective model to predict the poor prognosis of IPF.

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Section: Discussionmentioning

confidence: 99%

An 8-ferroptosis-related genes signature from Bronchoalveolar Lavage Fluid for prognosis in patients with idiopathic pulmonary fibrosis

Shang²,

et al. 2022

BMC Pulm Med

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“…MiR-27a-3p was also shown to target NFKB1 and thus, was suggested as a key regulator of M2 macrophage polarization ( 34 ). Recently, a study investigated the potential connections between arsenic and epigenetic changes that mediate M2 macrophage polarization in the development of PF and reported arsenite, elevated LncRNA H19, c-Myc, and Arg1 along with decreased let-7a to be associated with PF in mice ( 82 ). Another recent study in a mouse model reported MSC−derived exosomal miR−135b to promote M2 polarization of synovial macrophage by targeting MAPK6, thus mitigating cartilage injury ( 83 ).…”

Section: Microrna-based Regulation Of Macrophage Polarization In Immune Response Inflammation and Fibrosismentioning

confidence: 99%

Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis

2021

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This mini-review summarizes the current evidence for the role of macrophage activation and polarization in inflammation and immune response pertinent to interstitial lung disease, specifically pulmonary fibrosis. In the fibrosing lung, the production and function of inflammatory and fibrogenic mediators involved in the disease development have been reported to be regulated by the effects of polarized M1/M2 macrophage populations. The M1 and M2 macrophage phenotypes were suggested to correspond with the pro-inflammatory and pro-fibrogenic signatures, respectively. These responses towards tissue injury followed by the development and progression of lung fibrosis are further regulated by macrophage-derived microRNAs (miRNAs). Besides cellular miRNAs, extracellular exosomal-miRNAs derived from M2 macrophages have also been proposed to promote the progression of pulmonary fibrosis. In a future perspective, harnessing the noncoding miRNAs with a key role in the macrophage polarization is, therefore, suggested as a promising therapeutic strategy for this debilitating disease.

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“…Transforming growth factor beta (TGFβ) /Smad is recognized to be the most critical signalling pathway to induce fibrosis 8,9 . Regarding the upstream modulators of the TGFβ/Smad pathway, the long non‐coding RNAs (lncRNAs), including lncRNA LFAR1, 10 MEG3, 11 DNM3OS, 12 MIR503HG, 13 Erbb4‐IR, 14 and H19, 15 have been reported in the fibrosis of various organs 16‐18 …”

Section: Introductionmentioning

confidence: 99%

“…8,9 Regarding the upstream modulators of the TGFβ/Smad pathway, the long non-coding RNAs (lncRNAs), including lncRNA LFAR1, 10 MEG3, 11 DNM3OS, 12 MIR503HG, 13 Erbb4-IR, 14 and H19, 15 have been reported in the fibrosis of various organs. [16][17][18] As the first lncRNA found in skeletal muscle cell differentiation 19,20 and its function in regulating the TGFβ/Smad signalling pathway, 15 we suspected lnc-H19 might be involved in skeletal muscle fibrosis.Recently, lncRNAs were found to modulate mRNA-targeted genes expression at the post-transcriptional level by binding with microRNAs (miRNAs) in the cytoplasm 15,21 to act as competing endogenous RNA (ceRNA). Except from the nucleus, lnc-H19 was found to locate in the cytoplasm, and could operate as ceRNA.…”

mentioning

confidence: 97%

Long non‐coding RNA H19 promotes myoblast fibrogenesis via regulating the miR‐20a‐5p‐Tgfbr2 axis

Lin

Luo

Liu

et al. 2021

Clin Exp Pharma Physio

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Emerging evidence has indicated long non‐coding RNAs (lncRNAs) play important roles in diverse biological processes, including fibrosis. Here, we report that lncRNA H19 is able to promote skeletal muscle fibrosis. lnc‐H19 was identified to be highly expressed in skeletal muscle fibrosis in vivo and in vitro; while lnc‐H19 knockdown attenuated fibrosis in vitro. The knockdown of lnc‐H19 was proved to inhibit the activation of the TGFβ/Smad pathway in C2C12 myoblasts by sponging miR‐20a‐5p to regulate Tgfbr2 expression through the competing endogenous RNA function. Our study elucidates the roles of the lnc‐H19‐miR‐20a‐5p‐Tgfbr2 axis in regulating the TGFβ/Smad pathway of myoblast fibrogenesis, which might provide a promising therapeutic target for skeletal muscle fibrosis.

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LncRNA H19-mediated M2 polarization of macrophages promotes myofibroblast differentiation in pulmonary fibrosis induced by arsenic exposure

Cited by 58 publications

References 51 publications

An 8-ferroptosis-related genes signature from Bronchoalveolar Lavage Fluid for prognosis in patients with idiopathic pulmonary fibrosis

An 8-ferroptosis-related genes signature from Bronchoalveolar Lavage Fluid for prognosis in patients with idiopathic pulmonary fibrosis

Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis

Long non‐coding RNA H19 promotes myoblast fibrogenesis via regulating the miR‐20a‐5p‐Tgfbr2 axis

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