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Tytuł pozycji:

MicroRNA-92a serves as a risk factor in sepsis-induced ARDS and regulates apoptosis and cell migration in lipopolysaccharide-induced HPMEC and A549 cell injury.

Tytuł :
MicroRNA-92a serves as a risk factor in sepsis-induced ARDS and regulates apoptosis and cell migration in lipopolysaccharide-induced HPMEC and A549 cell injury.
Autorzy :
Xu F; Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China. Electronic address: .
Yuan J; Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China.
Tian S; Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China.
Chen Y; Emergency Department, Chongqing Emergency Medical Center, Chongqing 400016, PR China.
Zhou F; Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, PR China. Electronic address: .
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Źródło :
Life sciences [Life Sci] 2020 Sep 01; Vol. 256, pp. 117957. Date of Electronic Publication: 2020 Jun 10.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
MeSH Terms :
Apoptosis*/drug effects
Apoptosis*/genetics
Cell Movement*/drug effects
Cell Movement*/genetics
Endothelial Cells/*pathology
Lung/*blood supply
MicroRNAs/*metabolism
Respiratory Distress Syndrome, Adult/*etiology
Respiratory Distress Syndrome, Adult/*genetics
Sepsis/*complications
A549 Cells ; Aged ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Inflammation/pathology ; Intensive Care Units ; Lipopolysaccharides ; MicroRNAs/blood ; MicroRNAs/genetics ; Microvessels/pathology ; Middle Aged ; Proto-Oncogene Proteins c-akt/metabolism ; Respiratory Distress Syndrome, Adult/blood ; Respiratory Distress Syndrome, Adult/pathology ; Risk Factors ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Contributed Indexing :
Keywords: Acute respiratory distress syndrome; Akt/mTOR signal pathway; Apoptosis; Sepsis; miR-92a
Substance Nomenclature :
0 (Lipopolysaccharides)
0 (MIRN92 microRNA, human)
0 (MicroRNAs)
EC 2.7.1.1 (TOR Serine-Threonine Kinases)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
Entry Date(s) :
Date Created: 20200614 Date Completed: 20200831 Latest Revision: 20200831
Update Code :
20201023
DOI :
10.1016/j.lfs.2020.117957
PMID :
32534035
Czasopismo naukowe
Aims: Sepsis-induced acute respiratory distress syndrome (ARDS) is a common, high mortality complication in intensive care unit (ICU) patients. MicroRNA-92a (miR-92a) plays a role in many diseases, but its association with sepsis-induced ARDS is unclear.
Materials and Methods: We enrolled 53 patients, including 17 with sepsis only, and 36 with sepsis-induced ARDS. Lipopolysaccharide (LPS) was used to stimulate pulmonary microvascular endothelial cells (HPMEC) and alveolar epithelial A549 cells, which were used to investigate the miR-92a roles in ARDS. MiR-92a expression levels in patient serum and cells were quantified using quantitative reverse transcription-polymerase chain reaction (RT-PCR), and protein expression was examined using Western blotting. The effect of miR-92a on apoptosis was examined using flow cytometry. Wound healing and transwell migration assays were used to evaluate cell migration.
Key Findings: Serum miR-92a expression was higher in patients with sepsis-induced ARDS, when compared to patients with sepsis only. After LPS treatment in cells, miR-92a expression was higher when compared with control group, cell apoptosis and inflammatory responses were increased and cell migration was inhibited. However, cell apoptosis and inflammatory responses were decreased and cell migration was enhanced after miR-92a downregulation, when compared with inhibitor negative control (NC) group. Moreover, phosphorylated-Akt and phosphorylated-mTOR expression were increased after miR-92a inhibition.
Significance: Our study provides evidence that circulating serum miR-92a could act as a risk factor for sepsis-induced ARDS. MiR-92a inhibition attenuated the adverse effects of LPS on ARDS through the Akt/mTOR signaling pathway.
(Copyright © 2020 Elsevier Inc. All rights reserved.)

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