ArticleCytokine2010
Extracellular heat shock cognate protein 70 induces cardiac functional tolerance to endotoxin: differential effect on TNF-alpha and ICAM-1 levels in heart tissue.
Article in Cytokine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Sex as Biological Variable in Cardiac Mitochondrial Bioenergetic Responses to Acute Stress.International journal of molecular sciences · 2022Article
- Review
- Klotho suppresses the inflammatory responses and ameliorates cardiac dysfunction in aging endotoxemic mice.Oncotarget · 2017Article
- EF1A1/HSC70 Cooperatively Suppress Brain Endothelial Cell Apoptosis via Regulating JNK Activity.CNS neuroscience & therapeutics · 2016Article
- Modulation of cellular stress response via the erythropoietin/CD131 heteroreceptor complex in mouse mesenchymal-derived cells.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Gender disparity in the role of TLR2 in post-ischemic myocardial inflammation and injury.International journal of clinical and experimental medicine · 2015Article
- Article
- Enhanced monocyte chemoattractant protein-1 production in aging mice exaggerates cardiac depression during endotoxemia.Critical care (London, England) · 2014Article
- Human myocardium releases heat shock protein 27 (HSP27) after global ischemia: the proinflammatory effect of extracellular HSP27 through toll-like receptor (TLR)-2 and TLR4.Molecular medicine (Cambridge, Mass.) · 2014Article
- Sialyl-glycoconjugates in cholesterol-rich microdomains of P388 cells are the triggers for apoptosis induced by Rana catesbeiana oocyte ribonuclease.Glycoconjugate journal · 2014Article
- Article
- Heat shock protein 72 expressing stress in sepsis: unbridgeable gap between animal and human studies--a hypothetical "comparative" study.BioMed research international · 2014Review
- Identification of a heat shock cognate protein 70 gene in Chinese soft-shell turtle (Pelodiscus sinensis) and its expression profiles under thermal stress.Journal of Zhejiang University. Science. B · 2012Article
- Heat shock proteins: conditional mediators of inflammation in tumor immunity.Frontiers in immunology · 2012Article
- Heat shock proteins in stabilization of spontaneously restored sinus rhythm in permanent atrial fibrillation patients after mitral valve surgery.Cell stress & chaperones · 2011Article
- Oxidized low density lipoprotein induces bone morphogenetic protein-2 in coronary artery endothelial cells via Toll-like receptors 2 and 4.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endotoxin provokes cardiac dysfunction, and induction of tolerance to endotoxin has therapeutic potential. Heat shock protein 70 (HSP70) can induce endotoxin tolerance in macrophages. We recently found that heat shock cognate protein 70 (HSC70) induces pro-inflammatory cytokines via activation of TLR4 in macrophages and the myocardium. We hypothesize that HSC70 preconditioning induces cardiac tolerance to endotoxin. Pretreatment of peritoneal macrophages with HSC70 for 24h reduced TNF-alpha levels following endotoxin stimulation. Preconditioning of mice with HSC70 24h prior to endotoxin attenuated endotoxemic cardiac dysfunction. HSC70 preconditioning reduced TNF-alpha levels in plasma and heart tissue by 33.3% and 35.4%, respectively, and decreased ICAM-1 levels in heart tissue by 63.5% following endotoxin challenge. The effect of HSC70 on TNF-alpha was less robust than endotoxin preconditioning (79.7% and 75.0% reduction in TNF-alpha levels in plasma and heart tissue, respectively); however, HSC70 and endotoxin preconditioning had comparable effects on ICAM-1 levels in heart tissue. While HSC70 preconditioning had no effect on myocardial TLR4 protein levels, it suppressed NF-kappaB activation induced by endotoxin. We conclude that HSC70 preconditioning (1) attenuates the TNF-alpha response to endotoxin in macrophages in vitro, (2) induces cardiac functional tolerance to endotoxin and (3) reduces NF-kappaB activity, and TNF-alpha and ICAM-1 levels in heart tissue. Thus, the mechanism of HSC70-induced cardiac tolerance to endotoxin appears to involve down-regulation of myocardial TLR4 signaling and inflammatory responses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.