title: Nuclear factor-κB as a link between endoplasmic reticulum stress and inflammation during cardiomyocyte hypoxia/reoxygenation.
abstract: Endoplasmic reticulum stress (ERS) can initiate inflammation, and the coupling of these responses is thought to be fundamental to the pathogenesis of cardiovascular disease. However, the mechanism linking ERS and inflammation in myocardial ischemia/reperfusion needs further investigation. Cultured cardiomyocytes were pretreated with SP600125 or salubrinal, followed by tunicamycin to clarify the involvement of the IRE1α and PERK pathways in ERS inflammation. The cardiomyocytes were given hypoxia/reoxygenation (H/R), and the effects of the NF-κB inhibitor, SN50, were followed. GRP78 protein levels were similar in the tunicamycin (Tm), salubrinal, and SP600125 groups, but were lower in cells treated with SN50. SN50 might effectively block the H/R-induced link between ERS and inflammation in cardiomyocytes by decreasing GRP78. This knowledge will aid in the development of therapies for myocardial ischemia/reperfusion injury.
authors.affiliation: Department of Ophthalmology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, China.
authors.forename: Qin
authors.initials: Q
authors.lastname: Wu
authors.forename: Qiqi
authors.initials: Q
authors.lastname: Wang
authors.forename: Zhidong
authors.initials: Z
authors.lastname: Guo
authors.forename: Yunpeng
authors.initials: Y
authors.lastname: Shang
authors.forename: Lei
authors.initials: L
authors.lastname: Zhang
authors.forename: Shikun
authors.initials: S
authors.lastname: Gong
mesh_terms: D000818:Animals; D000873:Anthracenes / Q000494:pharmacology; D015687:Cell Hypoxia; D002478:Cells, Cultured; D002934:Cinnamates / Q000494:pharmacology; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects / Q000502:physiology*; D004722:Endoribonucleases / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D006360:Heat-Shock Proteins / Q000378:metabolism; D007249:Inflammation; D009097:Multienzyme Complexes / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D016328:NF-kappa B / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014415:Tunicamycin / Q000494:pharmacology; D019892:eIF-2 Kinase / Q000378:metabolism; D000091342:Endoplasmic Reticulum Chaperone BiP
chemical_list: D000873:Anthracenes; D002934:Cinnamates; D004722:Endoribonucleases; D006360:Heat-Shock Proteins; D009097:Multienzyme Complexes; D016328:NF-kappa B; D010455:Peptides; D017346:Protein Serine-Threonine Kinases; D013890:Thiourea; D014409:Tumor Necrosis Factor-alpha; D014415:Tunicamycin; D019892:eIF-2 Kinase; C575026:Ern1 protein, rat; C051684:GRP78 protein, rat; D000091342:Endoplasmic Reticulum Chaperone BiP; C118258:SN50 peptide; C496827:salubrinal; C432165:pyrazolanthrone
keywords: endoplasmic reticulum stress; hypoxia/reoxygenation; inflammation