ArticleMolecular & cellular toxicology2016
Expression profiling of microRNAs in lipopolysaccharide-induced acute lung injury after hypothermia treatment.
Article in Molecular & cellular toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 12 citations in OpenAlex.
- MiRNAs and Neutrophil-Related Membrane Proteins from Plasma-Derived Extracellular Vesicles for Early Prediction of Organ Dysfunction and Prognosis in Septic Patients.Journal of inflammation research · 2024Article
- Mechanism of chlorogenic acid reducing lipopolysaccharideZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Article
- Characterization of MicroRNA and Gene Expression Profiles Following Ricin Intoxication.Toxins · 2019Article
- Essential Oils as Repellents against Arthropods.BioMed research international · 2018Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the expression profiles of miRNAs in acute lung injury (ALI) rats after hypothermia treatment. ALI rats were induced with lipopolysaccharide (LPS) and maintained with hypothermia (HT) or normothermia (NT) for 6 hours. HT attenuated inflammatory cell infiltration in the lung and improved biochemical indicators of multi-organ dysfunction. Nineteen miRNAs were significantly differentially expressed in the HT group compared with the NT group. miR-142, miR-98, miR-541, miR-503, miR-653, miR- 223, miR-323 and miR-196b exhibited opposite patterns of expression between the two groups. These dysregulated miRNAs were mainly involved in the immune and inflammatory response on functional annotation analyses. This study shows that HT has lung protective effects and influences expression profiles of miRNAs in ALI. And dysregulated miRNAs after HT modulate the immune and inflammation in ALI. These results suggest that dysregulated miRNAs play a role in the mechanism of the lung protective effects of HT in ALI.
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