ArticleTransplantation2009
Human heat shock protein 27 overexpressing mice are protected against hepatic ischemia and reperfusion injury.
Article in Transplantation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Inflammatory Gene Expression in Livers Undergoing Ex Situ Normothermic Perfusion Is Attenuated by Leukocyte Removal From the Perfusate.Transplantation · 2025Article
- Review
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- Effect of Heat Shock Preconditioning on Pressure Injury Prevention via Hsp27 Upregulation in Rat Models.International journal of molecular sciences · 2022Article
- Transcriptional analysis identifies potential novel biomarkers associated with successful ex-vivo perfusion of human donor lungs.Clinical transplantation · 2022Article
- Literature review of the mechanisms of acute kidney injury secondary to acute liver injury.World journal of nephrology · 2022Review
- What is the role of heat shock protein in abdominal organ transplantation?Einstein (Sao Paulo, Brazil) · 2022Article
- Danger signals in liver injury and restoration of homeostasis.Journal of hepatology · 2020Review
- A1AR-mediated renal protection against ischemia/reperfusion injury is dependent on HSP27 induction.International urology and nephrology · 2018Article
- LPS ameliorates renal ischemia/reperfusion injury via Hsp27 up-regulation.International urology and nephrology · 2018Article
- Dietary ω-3 fatty acids protect against vasculopathy in a transgenic mouse model of sickle cell disease.Haematologica · 2015Article
- Comparative Study on the Cytoprotective Effects of Activated Protein C Treatment in Nonsteatotic and Steatotic Livers under Ischemia-Reperfusion Injury.BioMed research international · 2015Article
- Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.Molecular medicine reports · 2014Article
- Mitogen-activated protein kinase-activated protein kinase 2 mediates apoptosis during lung vascular permeability by regulating movement of cleaved caspase 3.American journal of respiratory cell and molecular biology · 2014Article
- Selective deletion of the endothelial sphingosine-1-phosphate 1 receptor exacerbates kidney ischemia-reperfusion injury.Kidney international · 2014Article
- Article
- Article
- Ischemia-induced apoptosis of intestinal epithelial cells correlates with altered integrin distribution and disassembly of F-actin triggered by calcium overload.Journal of biomedicine & biotechnology · 2012Article
- Tenascin-C: a novel mediator of hepatic ischemia and reperfusion injury.Hepatology (Baltimore, Md.) · 2011Article
- Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy.Laboratory investigation; a journal of technical methods and pathology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHepatic ischemia reperfusion injury (IRI) is a major clinical problem during the perioperative period and occurs frequently after major hepatic resection or liver transplantation. Our laboratory previously demonstrated that exogenous A1 adenosine receptor activation protects against renal IRI by upregulation and phosphorylation of heat shock protein 27 (HSP27).
methodsThis study used mice overexpressing human HSP27 (huHSP27 OE) to determine whether these mice are protected against liver IRI.
resultsAfter hepatic IR, the huHSP27 OE mice had significant protection against liver injury (reduced alanine transferase) and necrosis (hematoxylin-eosin staining) compared with the HSP27 WT mice. The huHSP27 OE mice also showed less induction of proinflammatory messenger RNA MIP-2, reduced neutrophil infiltration, and decreased apoptosis (caspase 3 fragmentation and DNA laddering) compared with the HSP27 WT mice. Finally, the huHSP27 OE mice showed significantly less disruption of filamentous actin in hepatocytes and bile canaliculi of the ischemic lobes compared with the HSP27 WT mice. Depletion of Kupffer cells with gadolinium chloride provided significant protection against liver IRI in HSP27 WT mice but not in huHSP27 OE mice suggesting that the overexpression of huHSP27 in the Kupffer cells may be responsible for the hepatic protection observed in huHSP27 OE mice.
conclusionsOur results show that the overexpression of huHSP27 in Kupffer cells of the liver may be responsible for the protection against hepatic IRI in vivo by reducing necrosis and apoptosis and by stabilizing F-actin with subsequent reductions in inflammation and proinflammatory neutrophil infiltration. Harnessing the mechanisms of cytoprotection with HSP27 may lead to new therapies for the management of perioperative hepatic IRI.
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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.