The mechanism and biomarker function of Cavin-2 in lung ischemia-reperfusion injury

Lung Ischemia Reperfusion injury(LIRI) is one of the most predominant complications of ischemic lung disease. Cavin-2 emerged as a regulator of a variety of cellular processes, including endocytosis, lipid homeostasis, signal transduction and tumorigenesis, but the function of Cavin-2 in LIRI is unk...

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Bibliographic Details
Published in:Computers in biology and medicine 2022-12, Vol.151 (Pt A), p.106234-106234, Article 106234
Main Authors: Tang, Hexiao, Sun, Linao, Huang, Jingyu, Yang, Zetian, Li, Changsheng, Zhou, Xuefeng
Format: Article
Language:English
Subjects:
AKT
AKT protein
Animal tissues
Animals
Biomarkers
Carbon dioxide
Cavin-2
Cell lines
Complications
Deep learning
Endocytosis
ERK1/2
Experiments
Extracellular signal-regulated kinase
Genes
Genomics
Health risks
Homeostasis
Hypoxia
Injuries
Interleukin 10
Interleukin 6
Ischemia
Kinases
Laboratory animals
Lipids
Lung - metabolism
Lung diseases
Lung ischemia reperfusion injury
Overexpression
Phosphorylation
Proteins
Proto-Oncogene Proteins c-akt - metabolism
Rats
Rats, Sprague-Dawley
Reagents
Reperfusion
Reperfusion Injury - genetics
Reperfusion Injury - metabolism
Signal processing
Signal transduction
STAT3
Stat3 protein
Tumor necrosis factor-TNF
Tumorigenesis
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Summary:Lung Ischemia Reperfusion injury(LIRI) is one of the most predominant complications of ischemic lung disease. Cavin-2 emerged as a regulator of a variety of cellular processes, including endocytosis, lipid homeostasis, signal transduction and tumorigenesis, but the function of Cavin-2 in LIRI is unknown. The purpose of this study was to determine the predictive potential of Cavin-2 in protecting lung ischemia-reperfusion injury and its corresponding mechanisms. We found the strong relationship between Cavin-2 and multiple immune-related genes by deep learning method. To reveal the mechanism of Cavin-2 in LIRI, the LIRI SD rat model was constructed to detect the expression of Cavin-2 in the lung tissue of SD rats after LIRI, and the expression of Cavin-2 in lung cell lines was also detected. The expression of IL-6, IL-10 and MDA in cells after Cavin-2 over-expression or knockdown was examined under hypoxic conditions. The expression levels of p-AKT, p-STAT3 and p-ERK1/2 were measured in over-expressing Cavin-2 cells under hypoxic-ischemia conditions, and then the corresponding blockers of AKT, STAT3 and ERK1/2 were given to verify, whether they play a protective role in LIRI. After hypoxia, the expression of Cavin-2 in rat lung tissues was significantly increased, and the cellular activity and IL-10 in Cavin-2 over-expressing cells were significantly higher than that of the control group, while IL-6 and MDA were significantly lower than that of the control group, while the above results were reversed in Cavin-2 knockdown cells; Meanwhile, the phosphorylation levels of AKT, STAT3, and ERK1/2 were significantly increased in Cavin-2 over-expression cells after hypoxia. When AKT, STAT3, and ERK1/2 specific blockers were given, they lost their protective effect against LIRI. Cavin-2 shows biomarker potential in protecting lung from ischemia-reperfusion injury through the survivor activating factor enhancement (SAFE) and reperfusion injury salvage kinase (RISK) pathway.
ISSN:0010-4825
1879-0534
DOI:10.1016/j.compbiomed.2022.106234