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Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

ABSTRACT: Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

PROVIDER: PRJNA944694 | ENA |

REPOSITORIES: ENA

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Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

Project description:Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

| PRJNA945441 | ENA

Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

Project description:Although plasma exosomal circular RNAs (circRNAs) are valuable biomarkers and therapeutic targets for various diseases, their role in intestinal I/R injury remains unknown. This study screens the expression profile of circRNAs in intestinal tissue exosomes collected from intestinal I/R mice.

2023-09-13 | GSE227355 | GEO

Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating hnRNPA1/Gprc5a signaling

Project description:To investigate the critical role of circEZH2_005 in regulating mRNA synthesis, stability, and translation, we evaluated intestinal crypt cells overexpressing circEZH2_005 by transcriptome sequencing.

2023-09-13 | GSE227518 | GEO

Exosomal circEZH2_005, an intestinal injury biomarker, alleviates intestinal ischemia/reperfusion injury by mediating Gprc5a signaling.

Project description:Intestinal ischemia/reperfusion (I/R) injury is a severe clinical condition without optimal diagnostic markers nor clear molecular etiological insights. Plasma exosomal circular RNAs (circRNAs) are valuable biomarkers and therapeutic targets for various diseases, but their role in intestinal I/R injury remains unknown. Here we screen the expression profile of circRNAs in intestinal tissue exosomes collected from intestinal I/R mice and identify circEZH2_005 as a significantly downregulated exosomal circRNA. In parallel, circEZH2_005 is also reduced in the plasma of clinical cardiac surgery patients who developed postoperative intestinal I/R injury. Exosomal circEZH2_005 displays a significant diagnostic value for intestinal injury induced by I/R. Mechanistically, circEZH2_005 is highly expressed in intestinal crypt cells. CircEZH2_005 upregulation promotes the proliferation of Lgr5+ stem cells by direct interaction with hnRNPA1, and enhanced Gprc5a stability, thereby alleviating I/R-induced intestinal mucosal damage. Hence, exosomal circEZH2_005 may serve as a biomarker for intestinal I/R injury and targeting the circEZH2_005/hnRNPA1/Gprc5a axis may be a potential therapeutic strategy for intestinal I/R injury.

| S-EPMC10482849 | biostudies-literature

Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

Project description:Gprc5a is a lung tumor suppressor gene. Gprc5a-knockout (ko) mice can develop spontaneous lung cancer and Gprc5a-ko mouse model is relevant to human lung cancer. Thus, exploration of the mechanisms underlying lung tumorigenesis in Gprc5a-ko mice would be very helpful for revealing those in human lung cancer. We used microarrays to detail the global gene expression profile that underlies oncogenesis by Gprc5a-knockout gene deletion in mouse tracheal epithelial cells. Wild type and gene-knockout mouse tracheal epithelial cells that were divided into two groups were used for RNA extraction.

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2010-04-13 | E-GEOD-21309 | biostudies-arrayexpress

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Project description:We have shown that Gprc5a-/- mice form Kras-mutant lung tumors spontaneously which is accelerated by tobacco carcinogen (NNK) exposure. We found in these mice that Lcn2 was distinctively up-regulated along the spectrum of Kras-mutant lung cancer development. To understand the role of Lcn2 in lung cancer pathogenesis, we generated Gprc5a-/-/Lcn2-/- mice and found that these animals have increased lung tumor devleopment following NNK compared to Gprc5a-/- animals with intact Lcn2. To understand these effects, we performed RNA-sequencing (RNA-Seq) of lung tissues from Gprc5a-/-/Lcn2-/- and Gprc5a-/- mice at baseline (prior to NNK exposure) and of tumor-bearing lungs from both groups at seven months post-NNK exposure.

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Expression data from Gprc5a wild type or knockout mouse tracheal epithelial cells (MTECs)

2013-10-29 | GSE51777 | GEO

Differential gene expression patterns in lung carcinogenesis mediated by loss of mouse tumor supressor Gprc5a

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2010-04-13 | GSE21309 | GEO

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