Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Comprehensive Bioinformatics Analysis of Lipopolysaccharide-Induced Altered Autophagy in Acute Lung Injury and Construction of Underlying Competing Endogenous RNA Regulatory Mechanism

Liu JY., Jiang YX., Zhang MY., Huo C., Yang YC., Ji XL.

Laboratory Study on Hip, published in Biomed Res Int (2021) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Biomed Res Int (2021)
Reported sample size
—
Source database
Europe PMC
PMID
34722769
PMCID
PMC8553468
DOI
10.1155/2021/6831770
Citations
6

Abstract (original English)

Background Acute lung injury (ALI) is a fatal syndrome frequently induced by lipopolysaccharide (LPS) released from the bacterial cell wall. LPS could also trigger autophagy of lung bronchial epithelial cell to relieve the inflammation, while the overwhelming LPS would impair the balance of autophagy consequently inducing serious lung injury. Methods We observed the autophagy variation of 16HBE, human bronchial epithelial cell, under exposure to different concentrations of LPS through western blot, immunofluorescence staining, and electron microscopy. Eight strands of 16HBE were divided into two groups upon 1000 ng/ml LPS stimulation or not, which were sent to be sequenced at whole transcriptome. Subsequently, we analyzed the sequencing data in functional enrichment, pathway analysis, and candidate gene selection and constructed a hsa-miR-663b-related competing endogenous RNA (ceRNA) network. Results We set a series of concentrations of LPS to stimulate 16HBE and observed the variation of autophagy in related protein expression and autophagosome count. We found that the effective concentration of LPS was 1000 ng/ml at 12 hours of exposure and sequenced the 1000 ng/ml LPS-stimulated 16HBE. As a result, a total of 750 differentially expressed genes (DEGs), 449 differentially expressed lncRNAs (DElncRNAs), 76 differentially expressed circRNAs (DEcircRNAs), and 127 differentially e

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cell LineHumansLipopolysaccharidesMicroRNAsRNA, MessengerPrognosisGene Expression ProfilingComputational BiologyGene ExpressionGene Expression Regulation, Neoplastic

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research