Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR‐485‐5p‐mediated CXCL10 inhibition

Chen, Yingwei; Chen, Xiaojie; Li, Haiyu; Liu, Yunpeng; Cheng, Dong; Tang, Yi; Sang, Haiqiang

doi:10.1002/ctm2.482

Cited by 30 publications

(18 citation statements)

References 35 publications

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“…A study has shown that CXCL10 can predict the prognosis of patients with advanced serous OV [39]. Increased CXCL10 expression promotes atrial fibrosis, inflammation, and oxidative stress [40]. A study has shown that FDCSP promotes the invasion and migration of OV cells [41].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Response Biomarkers of Ovarian Cancer Based on Single-Cell and Bulk RNA Sequencing

Zheng

Liu

et al. 2023

Oxidative Medicine and Cellular Longevity

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Background. The occurrence and development of ovarian cancer (OV) are significantly influenced by increased levels of oxidative stress (OS) byproducts and the lack of an antioxidant stress repair system. Hence, it is necessary to explore the markers related to OS in OV, which can aid in predicting the prognosis and immunotherapeutic response in patients with OV. Methods. The single-cell RNA-sequencing (scRNA-seq) dataset GSE146026 was retrieved from the Gene Expression Omnibus (GEO) database, and Bulk RNA-seq data were obtained from TCGA and GTEx databases. The Seurat R package and SingleR package were used to analyze scRNA-seq and to identify OS response-related clusters based on ROS markers. The “limma” R package was used to identify the differentially expressed genes (DEGs) between normal and ovarian samples. The risk model was constructed using the least absolute shrinkage and selection operator (LASSO) regression analysis. The immune cell infiltration, genomic mutation, and drug sensitivity of the model were analyzed using the CIBERSORT algorithm, the “maftools,” and the “pRRophetic” R packages, respectively. Results. Based on scRNA-seq data, we identified 12 clusters; OS response-related genes had the strongest specificity for cluster 12. A total of 151 genes were identified from 2928 DEGs to be significantly correlated with OS response. Finally, nine prognostic genes were used to construct the risk score (RS) model. The risk score model was an independent prognostic factor for OV. The gene mutation frequency and tumor immune microenvironment in the high- and low-risk score groups were significantly different. The value of the risk score model in predicting immunotherapeutic outcomes was confirmed. Conclusions. OS response-related RS model could predict the prognosis and immune responses in patients with OV and provide new strategies for cancer treatment.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress Response Biomarkers of Ovarian Cancer Based on Single-Cell and Bulk RNA Sequencing

Zheng

Liu

et al. 2023

Oxidative Medicine and Cellular Longevity

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“…There is emerging evidence that lncRNAs play pivotal roles in cardiovascular disease, including organ injury and fibrosis, development by functioning as ceRNAs to bind with miRNAs ( 44 , 45 ). For example, serum extracellular vesicles carrying lncRNA MIAT induce atrial injury, inflammation, and fibrosis to promote atrial remodeling and atrial fibrillation via sponging to miR-485-5p ( 46 ). The upregulation of lncRNA DCRF increases myocardial fibrosis, injury, and the acceleration of cardiomyocyte autophagy levels by acting as a ceRNA to sponge with miR-551b-5p ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

Enhancement of LncRNA-HFRL expression induces cardiomyocyte inflammation, proliferation, and fibrosis via the sequestering of miR-149-5p-mediated collagen 22A inhibition

Teng

Tian

et al. 2022

Ann Transl Med

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Background Long non-coding ribonucleic acids (lncRNAs) are believed to play crucial roles in cardiovascular diseases; however, details of the underlying mechanisms by which this occurs remain unclear. Methods A mouse heart failure (HF) model was established using isoproterenol (ISO), and confirmed by immunostaining and echocardiography. RNA-sequencing was performed to screen the differential lncRNA expression profiles and heart failure relative lncRNA (HFRL) was selected as the target which was validated by quantitative real-time polymerase chain reaction (qRT-PCR). In HL-1 cells, the cardiac function, inflammatory, and fibrosis-related genes expression changes were examined by qRT-PCR after silencing of HFRL by lentivirus. Meanwhile, Cell Counting Kit-8 (CCK-8) assays were used to detect the effects of HFRL on the cell proliferation and viability. Reactive oxygen species (ROS) assays were also used to explore the role of HFRL in oxidative damage. Next, bioinformatics analysis was conducted to predict the potential binding microRNAs (mmu-miR-149-5p) to HFRL, which was confirmed by RNA-pulldown assays. The target gene of miR-149-5p was also predicted and further validated by Dual-luciferase reporter assays, qRT-PCR, and western blot. To investigate the synergistic regulatory effect of HFRL and miR-149-5p, HL-1 cells were infected with the lentivirus of HFRL with or without simultaneous knockdown of miR-149-5p. Then, qRT-PCR and western blot were used to examine cardiac function, inflammatory, and fibrosis-related gene expression changes, respectively. In HL-1 cells, CCK-8 assays were performed to detect the proliferation and viability. ROS assays were used to explore the oxidative damage. Results The administration of ISO induced mice fibrosis, inflammation, and HF. The in-vitro results showed that knockdown of HFRL suppressed cardiomyocyte proliferation and viability, attenuated inflammatory, cardiac function, and fibrosis-related gene expression, and promoted oxidative damage. HFRL was found to bind to mmu-miR-149-5p and inversely target the 3'-untranscripted region of the collagen 22A1 gene. Thus, HFRL affected cardiomyocyte inflammation, proliferation, viability, oxidative damage, and pro-fibrotic function via sequestration to miR-149-5p. Conclusions The HFRL/miR-149-5p axis plays an important role in regulating cardiac inflammation, proliferation, and fibrosis via a synergistic effect, which suggests that HFRL might be a novel target for HF.

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“…At present, the research on the effect of mir-485-5p on the morphology and function of the cardiovascular system shows contradictory conclusions, which may be caused by the selection of different myocardial fibrosis models (24). Mir-485-5p promoted cardiac fibrosis in the isoproterenol-induced model, while mir-485-5p showed cardioprotection in the acute myocardial infarction model (25). Therefore, the role of mir-485-5p in cardiac fibrosis deserves further study.…”

Section: Mir-485-5p Inhibits the Activation Of Cardiac Fibroblastsmentioning

confidence: 99%

Mir-485-5p on the Morphology and Function of Cardiovascular System

Zhang

Nie

Liu

et al. 2022

Cell Mol Biol (Noisy-le-grand)

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Cardiovascular disease is a global problem that seriously endangers human health and life. At present, hypertension is considered to be a polygenic disease caused by the interaction of environmental factors and genetic factors. Various environmental factors have been proved to promote the occurrence and development of cardiovascular disease. MicroRNA (miR), as an essential gene regulatory factor in vivo, has been confirmed to participate in the regulation of many cell pathways, and its abnormal expression is closely related to a variety of human diseases. MiR-485-5p is located at 7q22.1, which has been proved to play an essential role in the tumor and cardiovascular system. Therefore, this paper discussed the mechanism of miR-485-5p on the morphology and function of the cardiovascular system. It is believed that miR-485-5p will impact the morphology and function of the cardiovascular system. Therefore, in the current study, 1655 unrelated patients with cardiovascular system diseases were simulated and analyzed based on the above background. A double luciferase reporter gene detection system verified the combination of miRNAs target recognition. The results showed that miR-485-5p significantly inhibited the luciferase activity of pGL-miR-wt but had no effect on pGL6-miR-mut. The lack of miR-485-5p can promote the activation of cardiac fibroblasts. The findings of this study can provide a new understanding and direction for the study of cardiovascular system morphology and function.

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Serum extracellular vesicles containing MIAT induces atrial fibrosis, inflammation and oxidative stress to promote atrial remodeling and atrial fibrillation via blockade of miR‐485‐5p‐mediated CXCL10 inhibition

Cited by 30 publications

References 35 publications

Oxidative Stress Response Biomarkers of Ovarian Cancer Based on Single-Cell and Bulk RNA Sequencing

Oxidative Stress Response Biomarkers of Ovarian Cancer Based on Single-Cell and Bulk RNA Sequencing

Enhancement of LncRNA-HFRL expression induces cardiomyocyte inflammation, proliferation, and fibrosis via the sequestering of miR-149-5p-mediated collagen 22A inhibition

Mir-485-5p on the Morphology and Function of Cardiovascular System

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