Construction and Analysis of a ceRNA Network in Cardiac Fibroblast During Fibrosis Based on in vivo and in vitro Data

Gao, Qingyuan; Zhang, Haifeng; Chen, Zhi-Teng; Li, Yuewei; Wang, Shaohua; Wen, Zheng; Xie, Yong; Mai, Jing-Ting; Wang, Jingfeng; Chen, Yangxin

doi:10.3389/fgene.2020.503256

Cited by 8 publications

(8 citation statements)

References 74 publications

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“…In the previous study, MALAT1 levels were lower in most EC specimens than in nontumor tissues, 46 and the MALAT1 rs664589 C > G polymorphism was associated with a significant increase in endometrial cancer risk 47 . In one study, depletion of LINC00511 could alleviate cardiac fibroblasts activation 48 . CARMN, as a basal lineage‐specific lncRNA, has been reported that control cell self‐renewal by regulating the downstream gene through the triplex formation and targeting the promoter region of Wnt10a 49 .…”

Section: Discussionmentioning

confidence: 89%

“…47 In one study, depletion of LINC00511 could alleviate cardiac fibroblasts activation. 48 CARMN, as a basal lineage-specific lncRNA, has been reported that control cell self-renewal by regulating the downstream gene through the triplex formation and targeting the promoter region of Wnt10a. 49 Zhao et al reported that high expression of LINC00648 in lung cancer patients indicates poor prognosis of patients, and participated in the signal pathways of the Hippo signaling pathway, transcriptional misregulation in cancer, MAPK signaling pathway, proteoglycans in cancer.…”

Section: Discussionmentioning

confidence: 99%

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Potential serum metabolites and long‐chain noncoding RNA biomarkers for endometrial cancer tissue

Hao

Lin

Liu

et al. 2022

J of Obstet and Gynaecol

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Background Endometrial carcinoma (EC) is one of the most common tumors in the female reproductive system. There are nearly 200 000 new cases every year. It is the third most common gynecological malignant tumor leading to female death. The incidence rate is closely related to lifestyle, and the incidence rate varies in different regions. The incidence rate of EC is ranking the first in the female reproductive system cancer just second only to breast, lung, and colorectal cancer in North America and Europe and the incidence rate of EC is only second, followed by breast cancer and cervical cancer in China. Purpose The potential metabolic markers of endometrial cancer were screened by liquid chromatograph mass spectrometer (LC‐MS), and the tissues of patients with hysteromyoma and endometrial cancer were sequenced to explore the relationship between the disease and change in the content of long‐chain noncoding RNA (lncRNA). Methods Serum and tissue samples were collected from patients with endometrial dysplasia, endometrial cancer stage I, and endometrial cancer stage III. The metabolites in all serum samples were extracted, and the metabolites in all samples were detected by LC–MS/MS technology. The Pareto‐scaling method was used for normalization, and the MetaboAnalyst 4.0 software was used for different analyses. The T test between groups showed that p ≤ 0.05 was regarded as the metabolite with a difference. Further, the function of differential metabolites was determined by metabolite function enrichment and co‐expression analysis. Meanwhile, the differentially expressed lncRNA was detected by Illumina second‐generation high‐throughput sequencing technology, and the expression was analyzed by DEGseq software. Different lncRNA were screened according to p < 0.05. LncRNA with significant differences were screened by p < 0.01, q < 0.001, fold change ≥2, and false discovery rate (FDR) ≤0.001. Results Through synthesis of T test, cluster heatmap, and ROC curve analysis, five biomarkers with potential diagnostic ability were obtained, including 2,3‐Pyridinedicarboxylic acid (area under the curve (AUC) = 0.69), Hematommic acid, ethyl ester (AUC = 0.69), Maltitol (AUC = 0.69), 13(S)‐HODE (AUC = 0.88), and D‐Mannitol (AUC = 0.69) had potential diagnostic ability between EC phase I versus EC phase III. At the same time, lncRNA sequencing results showed that when endometrial atypical hyperplasia continued to change, including LINC00511, PVT1, and IQCH‐AS1 (downregulated), and only changed significantly in the endometrial dysplasia group, including MALAT1, CARMN (downregulated) and LINC00648, BISPR, LINC01534, and LINC00930 (upregulated). Moreover, both differential metabolites and differential lncRNA were annotated to the lipid metabolism pathway, suggesting that this pathway played an important role in the occurrence and development of endometrial carcinoma. Conclusions It can combine the results of metabolomics and lncRNA sequencing to assist in the early diagnosis of endometrial precancerous lesions and endomet...

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Potential serum metabolites and long‐chain noncoding RNA biomarkers for endometrial cancer tissue

Hao

Lin

Liu

et al. 2022

J of Obstet and Gynaecol

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“…What is more, in a plasma proteome profiling, TGFBI has a potential role in extracellular matrix remodeling in fibrosis [32]. A recent study further confirmed that TGFBI and ADAM19 were associated with the TGF-β1 pathway and cardiac fibrosis [33]. Thus, TGFBI probably plays a role in myocardial fibrosis.…”

Section: Discussionmentioning

confidence: 92%

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Guan

Liu

Huang

et al. 2022

Computational and Mathematical Methods in Medicine

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Background. Transforming growth factor beta-induced protein (TGFBI, encoded by TGFBI gene), is an extracellular matrix protein, widely expressed in variety of tissues. It binds to collagens type I, II, and IV and plays important roles in the interactions of cell with cell, collagen, and matrix. It has been reported to be associated with myocardial fibrosis, and the latter is an important pathophysiologyical basis of atrial fibrillation (AF). However, the mechanism of TGFBI in AF remains unclear. We aimed to detect the potential mechanism of TGFBI in AF via bioinformatics analysis. Methods. The microarray dataset of GSE115574 was examined to detect the genes coexpressed with TGFBI from 14 left atrial tissue samples of AF patients. TGFBI coexpression genes were then screened using the R package. Using online analytical tools, we determined the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, Gene Ontology (GO) annotation, and protein-protein interaction (PPI) network of TGFBI and its coexpression genes. The modules and hub genes of the PPI-network were then identified. Another dataset, GSE79768 was examined to verify the hub genes. DrugBank was used to detect the potential target drugs. Results. In GSE115574 dataset, a total of 1818 coexpression genes (769 positive and 1049 negative) were identified, enriched in 120 biological processes (BP), 38 cellular components (CC), 36 molecular functions (MF), and 39 KEGG pathways. A PPI-network with average 12.2-degree nodes was constructed. The genes clustered in the top module constructed from this network mainly play a role in PI3K-Akt signaling pathway, viral myocarditis, inflammatory bowel disease, and platelet activation. CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 were identified and finally verified as the hub genes, mainly enriched in pathways like leukocyte transendothelial migration, PI3K-Akt signaling pathway, viral myocarditis, rheumatoid arthritis, and platelet activation. Pegcetacoplan, ocriplasmin, and carvedilol were the potential target drugs. Conclusions. We used microdataset to identify the potential functions and mechanisms of the TGFBI and its coexpression genes in AF patients. Our findings suggest that CXCL12, C3, FN1, COL1A2, ACTB, VCAM1, and MMP2 may be the hub genes.

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“…ADAM19 plays a role in cell–cell and cell–matrix interactions [ 35 ]. ADAM19 expression is increased in TGF-β1-induced alveolar epithelial cells [ 36 ] and is significantly associated with the TGF-β1 signaling pathway and the activation of cardiac fibroblasts and cardiac fibrosis [ 37 ]. A previous study found that ADAM19 was primarily expressed in renal proximal tubular epithelial cells [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Human umbilical cord mesenchymal stem cell-derived exosomal miR-335-5p attenuates the inflammation and tubular epithelial–myofibroblast transdifferentiation of renal tubular epithelial cells by reducing ADAM19 protein levels

et al. 2022

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Background Renal tubular epithelial–myofibroblast transdifferentiation (EMT) plays a key role in the regulation of renal fibrosis. Exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs) play a crucial role in alleviating renal fibrosis and injury. Additionally, hucMSC-derived exosomes contain numerous microRNAs (miRNAs). However, it is unclear whether mesenchymal stem cells can regulate the transforming growth factor (TGF)-β1-induced EMT of human renal tubular epithelial cells (RTECs) through exosomal miRNAs. Method HK-2, a human RTEC line, was co-treated with TGF-β1 and hucMSC-derived exosomes. Additionally, TGF-β1-treated HK-2 cells were transfected with a miR-335-5p mimic and disintegrin and metalloproteinase domain-containing protein 19 (ADAM19)-overexpression plasmid. miR-335-5p expression and ADAM19 protein and inflammation levels were measured via quantitative reverse transcription polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assays, respectively. Results TGF-β1 treatment changed the shape of HK-2 cells from a cobblestone morphology to a long spindle shape, accompanied by an increase in interleukin (IL)-6, tumor necrosis factor-α, IL-1β, collagen I, collagen III, α-smooth muscle actin, vimentin, and N-cadherin protein levels, whereas E-cadherin protein levels were reduced in these HK-2 cells, suggesting that TGF-β1 treatment induced the inflammation and EMT of HK-2 cells. HucMSC-exosomes improved the inflammation and EMT phenotype of TGF-β1-induced HK-2 cells by transferring miR-335-5p. miR-335-5p was found to bind the ADAM19 3′-untranslated region to reduce ADAM19 protein levels. Additionally, miR-335-5p improved the inflammation and EMT phenotype of HK-2 cells by reducing ADAM19 protein levels with TGF-β1 induction. Conclusions HucMSC-derived exosomal miR-335-5p attenuates the inflammation and EMT of HK-2 cells by reducing ADAM19 protein levels upon TGF-β1 induction. This study provides a potential therapeutic strategy and identifies targets for clinically treating renal fibrosis.

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Construction and Analysis of a ceRNA Network in Cardiac Fibroblast During Fibrosis Based on in vivo and in vitro Data

Cited by 8 publications

References 74 publications

Potential serum metabolites and long‐chain noncoding RNA biomarkers for endometrial cancer tissue

Potential serum metabolites and long‐chain noncoding RNA biomarkers for endometrial cancer tissue

Identification of the Potential Molecular Mechanism of TGFBI Gene in Persistent Atrial Fibrillation

Human umbilical cord mesenchymal stem cell-derived exosomal miR-335-5p attenuates the inflammation and tubular epithelial–myofibroblast transdifferentiation of renal tubular epithelial cells by reducing ADAM19 protein levels

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