Cleavage of cyclic AMP-responsive element-binding protein H aggravates myocardial hypoxia reperfusion injury in a hepatocyte-myocardial cell co-culture system.
Acute-Phase Reaction
/ immunology
Animals
Animals, Newborn
Cell Hypoxia
/ immunology
Cell Survival
/ immunology
Cells, Cultured
Coculture Techniques
Cyclic AMP Response Element-Binding Protein
/ genetics
Disease Models, Animal
Endoplasmic Reticulum Stress
/ immunology
Gene Knockdown Techniques
Heat-Shock Proteins
/ metabolism
Hepatocytes
/ immunology
Humans
Interleukin-6
/ metabolism
Liver
/ cytology
Myocardial Ischemia
/ immunology
Myocardium
/ cytology
Myocytes, Cardiac
/ immunology
Primary Cell Culture
RNA, Small Interfering
/ metabolism
Rats
Rats, Sprague-Dawley
Signal Transduction
/ immunology
Tumor Necrosis Factor-alpha
/ metabolism
Acute phase response
co-culture system
cyclic AMP-responsive element-binding protein H
endoplasmic reticulum stress
hypoxia/reoxygenation
inflammatory cytokine
myocardial hypoxia–reperfusion injury
Journal
The Journal of international medical research
ISSN: 1473-2300
Titre abrégé: J Int Med Res
Pays: England
ID NLM: 0346411
Informations de publication
Date de publication:
May 2020
May 2020
Historique:
entrez:
12
5
2020
pubmed:
12
5
2020
medline:
9
3
2021
Statut:
ppublish
Résumé
This study aimed to determine whether proinflammatory cytokines have an effect on myocardial cells (MCs) and hepatocytes during myocardial ischemia to induce cyclic AMP-responsive element-binding protein H (CREBH) cleavage, activate the acute phase response in the liver, and cause a superimposed injury in MCs. In this study, a hepatocyte-MC transwell co-culture system was used to investigate the relationship between myocardial hypoxia/reperfusion injury and CREBH cleavage. MCs and hepatocytes of neonatal rats were obtained from the ventricles and livers of Sprague-Dawley rats, respectively. MCs were inoculated into the lower chamber of transwell chambers for 12 hours under hypoxia. Levels of the endoplasmic reticulum stress protein glucose-regulated protein 78 in MCs, CREBH in hepatocytes, inflammatory factor (tumor necrosis factor-α and interleukin-6) levels, and cell viability were evaluated. The effect of CREBH knockdown was also studied using a CREBH-specific short hairpin RNA (Ad-CREBHi). We found that proinflammatory cytokines affect MCs and hepatocytes during myocardial ischemia to induce CREBH cleavage, activate the acute phase response in the liver, and cause superimposed injury in MCs. Expression of CREBH aggravates myocardial injury during myocardial ischemia.
Identifiants
pubmed: 32389049
doi: 10.1177/0300060520904835
pmc: PMC7221173
doi:
Substances chimiques
Creb3l3 protein, rat
0
Cyclic AMP Response Element-Binding Protein
0
GRP78 protein, rat
0
Heat-Shock Proteins
0
Il6 protein, rat
0
Interleukin-6
0
RNA, Small Interfering
0
Tumor Necrosis Factor-alpha
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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