MicroRNA-1 protects the endothelium in acute lung injury
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1001401 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25496600.fastq.gz | Fastqsanger.gz | |||
| SRR25496700.fastq.gz | Fastqsanger.gz | |||
| SRR25496601.fastq.gz | Fastqsanger.gz | |||
| SRR25496701.fastq.gz | Fastqsanger.gz | |||
| SRR25496602.fastq.gz | Fastqsanger.gz |
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Project description:MicroRNA-1 protects the endothelium in acute lung injury
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Project description:Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), cause severe endothelial dysfunction in the lung and vascular endothelial growth factor (VEGF) is elevated in ARDS. We have found that the levels of a VEGF-regulated microRNA, microRNA-1 (miR-1) is reduced in the lung endothelium after acute injury. Pulmonary endothelial cell (EC)-specific overexpression of miR-1 protects the lung against cell death and barrier dysfunction in both murine and human models and increases the survival of mice after pneumonia-induced ALI. MiR-1 has an intrinsic protective effect in pulmonary and other types of ECs; it inhibits apoptosis and necroptosis pathways and decreases capillary leak by protecting adherens and tight junctions. Comparative gene expression analysis and RISC recruitment assays identified miR-1 targets in the context of injury, including phosphodiesterase 5A (PDE5A), angiopoetin-2 (ANGPT2), connector enhancer of kinase suppressor of ras 3 (CNKSR3) and TNF alpha induced protein 2 (TNFAIP2). We validated miR-1-mediated regulation of ANGPT2 in both mouse and human ECs and found that in a 119-patient pneumonia cohort, miR-1 correlated inversely with ANGPT2. These findings illustrate the novel role of miR-1 as a cytoprotective orchestrator of endothelial response to acute injury with prognostic and therapeutic potential.
2023-10-25 | GSE236263 | GEO
Project description:Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), cause severe endothelial dysfunction in the lung and vascular endothelial growth factor (VEGF) is elevated in ARDS. We have found that the levels of a VEGF-regulated microRNA, microRNA-1 (miR-1) is reduced in the lung endothelium after acute injury. Pulmonary endothelial cell (EC)-specific overexpression of miR-1 protects the lung against cell death and barrier dysfunction in both murine and human models and increases the survival of mice after pneumonia-induced ALI. MiR-1 has an intrinsic protective effect in pulmonary and other types of ECs; it inhibits apoptosis and necroptosis pathways and decreases capillary leak by protecting adherens and tight junctions. Comparative gene expression analysis and RISC recruitment assays identified miR-1 targets in the context of injury, including phosphodiesterase 5A (PDE5A), angiopoetin-2 (ANGPT2), connector enhancer of kinase suppressor of ras 3 (CNKSR3) and TNF alpha induced protein 2 (TNFAIP2). We validated miR-1-mediated regulation of ANGPT2 in both mouse and human ECs and found that in a 119-patient pneumonia cohort, miR-1 correlated inversely with ANGPT2. These findings illustrate the novel role of miR-1 as a cytoprotective orchestrator of endothelial response to acute injury with prognostic and therapeutic potential.
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Project description:MicroRNA expression profiling in acute kidney injury
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Project description:Acute lung injury (ALI) and its most severe form, acute respiratory distress syndrome (ARDS), cause severe endothelial dysfunction in the lung, and vascular endothelial growth factor (VEGF) is elevated in ARDS. We found that the levels of a VEGF-regulated microRNA, microRNA-1 (miR-1), were reduced in the lung endothelium after acute injury. Pulmonary endothelial cell-specific (EC-specific) overexpression of miR-1 protected the lung against cell death and barrier dysfunction in both murine and human models and increased the survival of mice after pneumonia-induced ALI. miR-1 had an intrinsic protective effect in pulmonary and other types of ECs; it inhibited apoptosis and necroptosis pathways and decreased capillary leak by protecting adherens and tight junctions. Comparative gene expression analysis and RISC recruitment assays identified miR-1 targets in the context of injury, including phosphodiesterase 5A (PDE5A), angiopoietin-2 (ANGPT2), CNKSR family member 3 (CNKSR3), and TNF-α-induced protein 2 (TNFAIP2). We validated miR-1-mediated regulation of ANGPT2 in both mouse and human ECs and found that in a 119-patient pneumonia cohort, miR-1 correlated inversely with ANGPT2. These findings illustrate a previously unknown role of miR-1 as a cytoprotective orchestrator of endothelial responses to acute injury with prognostic and therapeutic potential.
| S-EPMC10561733 | biostudies-literature
Project description:Background: Acute kidney injury (AKI) is a common clinical event with high morbidity and mortality. We previously demonstrated that injection of cord blood endothelial colony forming cell (ECFC)-derived exosomes, highly enriched in miRNA(miR)-486-5p, prevented ischemic kidney injury in mice. While preclinical models support involvement of several miRs in AKI, the direct effects of miR-486-5p on injury and the kidney transcriptome are unknown. Objective: We studied effects of miR-486-5p in mice with kidney ischemia-reperfusion (IR) injury, and compared the impact of miR-486-5p and ECFC-derived exosomes on the transcriptome of proximal tubules (PTs) and renal endothelial cells. Methods: Adult male mice were subjected to bilateral kidney ischemia (30 min), and injected via tail vein with or without vehicle, miR-486-5p mimic, ECFC-derived exosomes, or scramble miR at the start of reperfusion. Plasma and tissues were collected 24 hrs after reperfusion, and proximal tubular and endothelial cells were isolated for mRNA analysis by RNA-Seq. Results: In mice with kidney IR, injection of miR-486-5p mimic increased levels of miR-486-5p in proximal tubules and endothelial cells, and significantly improved plasma creatinine, histological injury, neutrophil infiltration, and apoptosis, compared to vehicle treatment. MiR-486-5p inhibited expression of phosphatase and tensin homolog (PTEN), and activated AKT. Similar results were observed with exosomes, but scramble miR had no effect. In proximal tubules, miR-486-5p or exosomes reduced expression of several AKI genes (e.g. Lcn2, Havcr1 and Krt20) and caused alterations in apoptotic genes compared to IR alone. In endothelium, miR-486-5p or exosomes caused milder effect than in PTs but still impacting on expression of injury-related genes. Conclusion: MiR-486-5p protects mice against ischemic kidney injury. Both miR-486-5p and exosomes reduce expression of apoptotic genes in PTs and endothelium. The results suggest that systemic delivery of miR-486-5p has therapeutic potential in ischemic AKI.
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Project description:The goal of this observational study is to compare anesthetic modalities (intravenous propofol anesthesia with sevoflurane gas anesthesia) in patients who underwent colorectal cancer resection surgery regarding the outcome of acute kidney injury.
The main questions it aims to answer are:
* is there a difference in acute kidney injury incidence in the two anesthetic modalities?
* is there a difference in plasma creatinine between the two anesthetic modalities?
* are there any patient characteristics or intraoperative factors that effect the incidence of acute kidney injury in either anesthetic modality?
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