Alternative RNA splicing and alternative transcription start/end in acute respiratory distress syndrome.
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ABSTRACT:
SUBMITTER: Fredericks AM
PROVIDER: S-EPMC7490973 | biostudies-literature | 2020 Apr
REPOSITORIES: biostudies-literature
Publications
Alternative RNA splicing and alternative transcription start/end in acute respiratory distress syndrome.
Fredericks Alger M AM Wang Li Juan LJ Fairbrother William G WG Ayala Alfred A Monaghan Sean F SF
Intensive care medicine 20200220 4
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Project description:Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) are at an increased risk of developing severe acute respiratory distress syndrome (ARDS), which is characterized by peripheral bilateral patchy lung involvement. The regulatory network of RNA-binding protein (RBP)-alternative splicing (AS) in ARDS following HSCT has not been investigated. We hypothesize that RBP-AS plays a regulatory role during HSCT-ARDS. The published ARDS transcriptome data after HSCT (GSE84439) were downloaded, and the transcriptome data of 13 mRNAs were obtained by sequencing the peripheral blood of 5 HSCT-ARDS patients and 8 ARDS patients through high-throughput sequencing technology. Systematic analysis of downloaded data was performed to obtain differentially expressed RBPs, and the differentially alternative spliced pre-mRNAs in HSCT-ARDS and control groups were used to explore the global gene RBP-AS regulatory network. A total of 1769 differentially expressed genes and 4714 regulated alternative splicing events were identified in peripheral blood from HSCT-ARDS, of which 254 genes had both differential expression and differential AS. In addition, 128 RBPs were identified, of which HDGF, PCBP2, RIOK3, CISD2, and TRIM21, DDX58, MOV10 showed significantly increased or decreased expression in the HSCT-ARDS. RBPs with decreased expression had antiviral activity, while those with increased expression were involved in ROS, fibrosis, and negative viral resistance. The RBP-RASE-RASG regulatory network is constructed. It is related to the dysregulation of antiviral immunomodulation, imbalance in ROS homeostasis and pro-pulmonary fibrosis, which are involved in the development of HSCT-ARDS.
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Project description:The acute respiratory distress syndrome (ARDS) is a common cause of respiratory failure in critically ill patients and is defined by the acute onset of noncardiogenic pulmonary oedema, hypoxaemia and the need for mechanical ventilation. ARDS occurs most often in the setting of pneumonia, sepsis, aspiration of gastric contents or severe trauma and is present in ~10% of all patients in intensive care units worldwide. Despite some improvements, mortality remains high at 30-40% in most studies. Pathological specimens from patients with ARDS frequently reveal diffuse alveolar damage, and laboratory studies have demonstrated both alveolar epithelial and lung endothelial injury, resulting in accumulation of protein-rich inflammatory oedematous fluid in the alveolar space. Diagnosis is based on consensus syndromic criteria, with modifications for under-resourced settings and in paediatric patients. Treatment focuses on lung-protective ventilation; no specific pharmacotherapies have been identified. Long-term outcomes of patients with ARDS are increasingly recognized as important research targets, as many patients survive ARDS only to have ongoing functional and/or psychological sequelae. Future directions include efforts to facilitate earlier recognition of ARDS, identifying responsive subsets of patients and ongoing efforts to understand fundamental mechanisms of lung injury to design specific treatments.
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Project description:Acute respiratory distress syndrome (ARDS) is an acute respiratory illness characterised by bilateral chest radiographical opacities with severe hypoxaemia due to non-cardiogenic pulmonary oedema. The COVID-19 pandemic has caused an increase in ARDS and highlighted challenges associated with this syndrome, including its unacceptably high mortality and the lack of effective pharmacotherapy. In this Seminar, we summarise current knowledge regarding ARDS epidemiology and risk factors, differential diagnosis, and evidence-based clinical management of both mechanical ventilation and supportive care, and discuss areas of controversy and ongoing research. Although the Seminar focuses on ARDS due to any cause, we also consider commonalities and distinctions of COVID-19-associated ARDS compared with ARDS from other causes.
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Project description:Bronchoalveolar Lavage Fluid protein profile was characterized in ARDS subjects. Patients were divided into three groups: 1) Early phase survivors 2) Early phase non-survivors and 3) Late phase survivors. Bronchoalveolar lavage fluid was pooled within each group for sample preparation and mass spectrometry
2016-07-07 | PXD001095 | Pride
Project description:Acute respiratory distress syndrome (ARDS) alveolar environment induced a pro-repair anti-inflammatory macrophage polarization. However, patients with coronavirus disease 2019 (COVID-19) ARDS frequently exhibit a huge lung inflammation and present pulmonary scars and fibrosis more frequently than patients with non-COVID-19 ARDS, suggesting that the COVID-19 ARDS alveolar environment may drive a more inflammatory or pro-fibrotic macrophage polarization. This study aimed to determine the effect of the COVID-19 ARDS alveolar environment on macrophage polarization. The main finding was that broncho-alveolar lavage fluids (BALF) from patients with early COVID-19 ARDS drove an alternative anti-inflammatory polarization in normal monocyte-derived macrophages; characterized by increased expressions of CD163 and CD16 mRNA (3.4 [2.7-7.2] and 4.7 [2.6-5.8] fold saline control, respectively - p = 0.02), and a secretory pattern close to that of macrophages stimulated with IL-10, with the specificity of an increased production of IL-6. This particular alternative pattern was specific to early ARDS (compared with late ARDS) and of COVID-19 ARDS (compared with moderate COVID-19). The early COVID-19 ARDS alveolar environment drives an alternative anti-inflammatory macrophage polarization with the specificity of inducing macrophage production of IL-6.
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Project description:The acute respiratory distress syndrome (ARDS) is an important cause of acute respiratory failure that is often associated with multiple organ failure. Several clinical disorders can precipitate ARDS, including pneumonia, sepsis, aspiration of gastric contents, and major trauma. Physiologically, ARDS is characterized by increased permeability pulmonary edema, severe arterial hypoxemia, and impaired carbon dioxide excretion. Based on both experimental and clinical studies, progress has been made in understanding the mechanisms responsible for the pathogenesis and the resolution of lung injury, including the contribution of environmental and genetic factors. Improved survival has been achieved with the use of lung-protective ventilation. Future progress will depend on developing novel therapeutics that can facilitate and enhance lung repair.
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Project description:Rat model of ARDS was induced by saline lavage and mechanical ventilation. Total RNA from rat lungs were used for dual color DNA microarray hybridization with 3DNA 50 kit version 2. Two-condition experiment, CON vs. ARDS lung tissues. replicates: 5 control, 7 ARDS. One replicate per array.
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