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Project description:Circular RNAs (circRNAs) are crucially involved in cancers as competing endogenous RNA (ceRNA) or microRNA (miRNA) sponges. However, the function and mechanism of circRNAs in liver fibrosis remain unknown and are the focus of this study. Murine fibrotic models were induced by thioacetamide (TAA) or carbon tetrachloride (CCl4 ). Increased angiogenesis is accompanied by liver fibrosis in TAA- and CCl4 -induced murine fibrotic livers. circRNA microarray and argonaute 2 (AGO2)-RNA immunoprecipitation (RIP) sequencing (AGO2-RIP sequencing) were performed in murine livers to screen for functional circRNAs. Compared to control livers, 86 differentially expressed circRNAs were obtained in TAA-induced murine fibrotic livers using circRNA microarray. In addition, 551 circRNAs were explored by AGO2-RIP sequencing of murine fibrotic livers. The circRNA-007371 was then selected and verified for back-spliced junction, resistance to RNase R, and loop formation. In vitro, murine hemangioendothelioma endothelial (EOMA) cells were transfected with circRNA-007371 overexpressing plasmid or empty plasmid. circRNA-007371 overexpression promoted tube formation, migration, and cell proliferation of EOMA cells. RNA sequencing and miRNA sequencing were then performed to explore the mechanism of the proangiogenic effects of circRNA-007371. circRNA-007371 promotes liver fibrosis via miRNA sponges or ceRNA mechanisms. Stag1, the parent gene of circRNA-007371, may play a significant role in proangiogenic progression. In conclusion, circRNA-007371 enhances angiogenesis via a miRNA sponge mechanism in liver fibrosis. The antiangiogenic effect of circRNA-007371 inhibition may provide a new strategy for treating patients with liver cirrhosis.
| S-EPMC10280135 | biostudies-literature
Project description:Objective Circular RNAs (circRNAs) are covalently closed, endogenous non-coding RNAs. CircRNAs play a vital role in liver diseases, acting as microRNA (miRNA) sponges. However, the angiogenic role of circRNA remains unknown in liver fibrosis and is the focus of this study. Methods Liver fibrosis was induced by thioacetamide (TAA), or carbon tetrachloride (CCl4) in mice. CircRNA-microarray, AGO2-RNA immunoprecipitation (RIP), and RNA-seq were utilized to explore the hepatic circRNAs profile. The qPCR and PCR-gel electrophoresis analysis were used to investigate the characterization of circRNA-007371. Liver tissues and EMOA murine endothelial cells were used to verify the angiogenic mechanism of circRNA-007371. Results The increased collagen deposition, pseudolobule formation, and angiogenesis were observed in murine liver induced by TAA and CCl4. CircRNA-microarray in TAA-induced fibrotic murine liver indicated that the expression of circRNA-007371 was up-regulated. Moreover, AGO2-RIP and PCR analysis showed that circRNA-007371 had the characterization of circRNAs and played a role as competing endogenous RNAs (ceRNA) sponging miR-200a. In vitro, circRNA-007371 promoted the ability of migration, growth, and blood vessel formation in EMOA murine endothelial cells using wound healing and tube formation assay. The AGO2-RIP and RNA-sequencing analysis in overexpression circRNA-007371 EMOA murine endothelial cells demonstrated that circRNA-007371 upregulates the stromal antigen 1 (Stag1) via spouse of miR-200a and HIF-1 signaling pathway might participate in the angiogenesis. Conclusions This study discovers that circRNA-007371, a novel ceRNA, is up-regulated, and enhances the angiogenesis via angiocrine role to regulate the STAG1-miR-200a-5p signaling pathway in liver fibrosis.
2023-06-28 | GSE218574 | GEO
Project description:Objective Circular RNAs (circRNAs) are covalently closed, endogenous non-coding RNAs. CircRNAs play a vital role in liver diseases, acting as microRNA (miRNA) sponges. However, the angiogenic role of circRNA remains unknown in liver fibrosis and is the focus of this study. Methods Liver fibrosis was induced by thioacetamide (TAA), or carbon tetrachloride (CCl4) in mice. CircRNA-microarray, AGO2-RNA immunoprecipitation (RIP), and RNA-seq were utilized to explore the hepatic circRNAs profile. The qPCR and PCR-gel electrophoresis analysis were used to investigate the characterization of circRNA-007371. Liver tissues and EMOA murine endothelial cells were used to verify the angiogenic mechanism of circRNA-007371. Results The increased collagen deposition, pseudolobule formation, and angiogenesis were observed in murine liver induced by TAA and CCl4. CircRNA-microarray in TAA-induced fibrotic murine liver indicated that the expression of circRNA-007371 was up-regulated. Moreover, AGO2-RIP and PCR analysis showed that circRNA-007371 had the characterization of circRNAs and played a role as competing endogenous RNAs (ceRNA) sponging miR-200a. In vitro, circRNA-007371 promoted the ability of migration, growth, and blood vessel formation in EMOA murine endothelial cells using wound healing and tube formation assay. The AGO2-RIP and RNA-sequencing analysis in overexpression circRNA-007371 EMOA murine endothelial cells demonstrated that circRNA-007371 upregulates the stromal antigen 1 (Stag1) via spouse of miR-200a and HIF-1 signaling pathway might participate in the angiogenesis. Conclusions This study discovers that circRNA-007371, a novel ceRNA, is up-regulated, and enhances the angiogenesis via angiocrine role to regulate the STAG1-miR-200a-5p signaling pathway in liver fibrosis.
2023-06-28 | GSE218578 | GEO
Project description:Objective Circular RNAs (circRNAs) are covalently closed, endogenous non-coding RNAs. CircRNAs play a vital role in liver diseases, acting as microRNA (miRNA) sponges. However, the angiogenic role of circRNA remains unknown in liver fibrosis and is the focus of this study. Methods Liver fibrosis was induced by thioacetamide (TAA), or carbon tetrachloride (CCl4) in mice. CircRNA-microarray, AGO2-RNA immunoprecipitation (RIP), and RNA-seq were utilized to explore the hepatic circRNAs profile. The qPCR and PCR-gel electrophoresis analysis were used to investigate the characterization of circRNA-007371. Liver tissues and EMOA murine endothelial cells were used to verify the angiogenic mechanism of circRNA-007371. Results The increased collagen deposition, pseudolobule formation, and angiogenesis were observed in murine liver induced by TAA and CCl4. CircRNA-microarray in TAA-induced fibrotic murine liver indicated that the expression of circRNA-007371 was up-regulated. Moreover, AGO2-RIP and PCR analysis showed that circRNA-007371 had the characterization of circRNAs and played a role as competing endogenous RNAs (ceRNA) sponging miR-200a. In vitro, circRNA-007371 promoted the ability of migration, growth, and blood vessel formation in EMOA murine endothelial cells using wound healing and tube formation assay. The AGO2-RIP and RNA-sequencing analysis in overexpression circRNA-007371 EMOA murine endothelial cells demonstrated that circRNA-007371 upregulates the stromal antigen 1 (Stag1) via spouse of miR-200a and HIF-1 signaling pathway might participate in the angiogenesis. Conclusions This study discovers that circRNA-007371, a novel ceRNA, is up-regulated, and enhances the angiogenesis via angiocrine role to regulate the STAG1-miR-200a-5p signaling pathway in liver fibrosis.
2023-06-28 | GSE218579 | GEO
Project description:Objective Circular RNAs (circRNAs) are covalently closed, endogenous non-coding RNAs. CircRNAs play a vital role in liver diseases, acting as microRNA (miRNA) sponges. However, the angiogenic role of circRNA remains unknown in liver fibrosis and is the focus of this study. Methods Liver fibrosis was induced by thioacetamide (TAA), or carbon tetrachloride (CCl4) in mice. CircRNA-microarray, AGO2-RNA immunoprecipitation (RIP), and RNA-seq were utilized to explore the hepatic circRNAs profile. The qPCR and PCR-gel electrophoresis analysis were used to investigate the characterization of circRNA-007371. Liver tissues and EMOA murine endothelial cells were used to verify the angiogenic mechanism of circRNA-007371. Results The increased collagen deposition, pseudolobule formation, and angiogenesis were observed in murine liver induced by TAA and CCl4. CircRNA-microarray in TAA-induced fibrotic murine liver indicated that the expression of circRNA-007371 was up-regulated. Moreover, AGO2-RIP and PCR analysis showed that circRNA-007371 had the characterization of circRNAs and played a role as competing endogenous RNAs (ceRNA) sponging miR-200a. In vitro, circRNA-007371 promoted the ability of migration, growth, and blood vessel formation in EMOA murine endothelial cells using wound healing and tube formation assay. The AGO2-RIP and RNA-sequencing analysis in overexpression circRNA-007371 EMOA murine endothelial cells demonstrated that circRNA-007371 upregulates the stromal antigen 1 (Stag1) via spouse of miR-200a and HIF-1 signaling pathway might participate in the angiogenesis. Conclusions This study discovers that circRNA-007371, a novel ceRNA, is up-regulated, and enhances the angiogenesis via angiocrine role to regulate the STAG1-miR-200a-5p signaling pathway in liver fibrosis.
2023-06-28 | GSE218577 | GEO
Project description:The angiogenic role of circRNA-007371 in liver fibrosis
| PRJNA904343 | ENA
Project description:The angiogenic role of circRNA-007371 in liver fibrosis [circRNA Microarray]
| PRJNA904333 | ENA
Project description:The angiogenic role of circRNA-007371 in liver fibrosis [RNA-Seq]
| PRJNA904349 | ENA
Project description:The angiogenic role of circRNA-007371 in liver fibrosis [RIP-Seq]
| PRJNA904350 | ENA
Project description:The angiogenic role of circRNA-007371 in liver fibrosis [ncRNA-Seq]
| PRJNA904351 | ENA