Release and activity of histone in diseases

Chen, R; Kang, Rui; Xg, Fan; Tang, Daolin

doi:10.1038/cddis.2014.337

Cited by 356 publications

(393 citation statements)

References 82 publications

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“…Histone is a highly conserved eukaryotic chromosomal protein. Under oxidative or inflammatory stress, histone undergoes translocation from the nucleus to the cytoplasm, and then it is secreted from the necrotic cells 11. In the liver, histone has been shown to mediate hepatocyte cell death and inflammation 12, 13.…”

Section: Introductionmentioning

confidence: 99%

VEGF mitigates histone-induced pyroptosis in the remote liver injury associated with renal allograft ischemia–reperfusion injury in rats

Zhao

Huang

Alam

et al. 2018

American Journal of Transplantation

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Clinical evidence has indicated a possible link between renal injury and remote liver injury. We investigated whether extracellular histone mediates remote hepatic damage after renal graft ischemia–reperfusion injury, while vascular endothelial growth factor (VEGF) is protective against remote hepatic injury. In vitro, hepatocyte HepG2 cultures were treated with histone. In vivo, the Brown‐Norway renal graft was stored in 4°C preservation solution for 24 hours and then transplanted into a Lewis rat recipient; blood samples and livers from recipients were harvested 24 hours after surgery. Prolonged cold ischemia in renal grafts enhanced liver injury 24 hours after engraftment. Caspase‐1, ASC, NLRP3, and AIM2 expressions in hepatocyte, CD68+‐infiltrating macrophages, tissue, and serum interleukin‐1β and ‐18 were greatly elevated, indicating that pyroptosis occurred in the liver and resulted in acute liver functional impairment. Blocking the caspase‐1 pathway decreased the number of necrotic hepatocytes. VEGF treatment suppressed the hepatocyte pyroptosis and liver function was partially restored. Our data suggested that renal allograft ischemia–reperfusion injury is likely associated with acute liver damage due to hepatocyte pyroptosis induced by histone and such injury may be protected by VEGF administration. VEGF, therefore, may serve as a new strategy against other remote organ injuries related to renal transplantation.

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Section: Introductionmentioning

confidence: 99%

VEGF mitigates histone-induced pyroptosis in the remote liver injury associated with renal allograft ischemia–reperfusion injury in rats

Zhao

Huang

Alam

et al. 2018

American Journal of Transplantation

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“…However, the same research demonstrated that NETs can deviate from the role of infection control, namely that immunothrombosis can induce damage to the host tissue through abnormal activation of the coagulation and immune systems, which can lead to MOF (14). In addition, NETs have components containing proteins that lead to tissue and endothelial damage as damageassociated molecular patterns (DAMPs) (15).…”

Section: Detachment Furthermore the Presence Of Extravasated Platelmentioning

confidence: 99%

Role for Neutrophil Extracellular Traps (NETs) and Platelet Aggregation in Early Sepsis-induced Hepatic Dysfunction

Sakurai

Miyashita

Okazaki

et al. 2017

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Abstract. Background Sepsis is a clinical syndrome of systemic inflammatory responses arising from an infectious process with a presumed or known focus (1, 2). Severe sepsis, defined as sepsis with acute organ dysfunction, is associated with high morbidity and mortality rates (3). Inflammation and coagulation play pivotal roles in the pathogenesis of sepsis (4, 5). Sepsis-induced multiple organ failure (MOF) has numerous causes, such as various types of shock, adult respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC) (6). Gando et al. (7) reported that DIC is frequently associated with systemic inflammatory response syndrome (SIRS; 83%) and that such patients have a high mortality rate (63%). Ogura et al. (4) evaluated coagulation activity, organ dysfunction, and SIRS in critically-ill patients with thrombocytopenia and examined the balance between coagulopathy and systemic inflammation. In critically-ill patients with thrombocytopenia, they found that coagulopathy and organ dysfunction progressed with a significant mutual correlation, depending on the increase in SIRS scores. Thus, SIRSassociated coagulopathy may play a critical role in inducing organ dysfunction after severe insult. 1051This article is freely accessible online.Correspondence to: Tomoharu Miyashita,

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“…Activation of TLRs (for example, TLR2, TLR4 and TLR9) and NLRP3 inflammasome mediate the activity of histones (87,89,145,148). Dynamic changes in circulating levels of histones as well as nucleosomes serve as potential biomarkers and novel therapeutic targets in human diseases (149,150).…”

Section: Histone and Acute Pancreatitismentioning

confidence: 99%

Cell Death and DAMPs in Acute Pancreatitis

Kang

Lotze

Zeh

et al. 2014

Mol Med

129

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The pancreas is a dual-purpose gland with exocrine and endocrine functions. The exocrine pancreas produces digestive proteases in inactive proenzyme form, namely zymogens. The pancreas is normally able to protect itself from zymogen activation by synthesis of protease inhibitors such as pancreatic secretory trypsin inhibitor and serine protease inhibitor (for example, SPINK1/Spink3). By contrast, pancreatic autodigestion and subsequent AP is initiated once these defenses are impaired. In studies of rodent models (for example, repetitive cerulein or L-arginine injections, choline-deficient ethionine supplementation [CDE] diet, perfusion of taurocholate into the biliary or pancreatic duct and surgical ligation or infusion of pancreatic duct models), some essential pathogenic AP events have been identified (see Figure 1) (15,16).The development of AP involves a complex cascade of events (17), which start with injury or disruption of the pan- Cell Death and DAMPs in Acute PancreatitisRui Kang, Michael T Lotze, Herbert J Zeh, Timothy R Billiar, and Daolin Tang Department of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America Cell death and inflammation are key pathologic responses of acute pancreatitis (AP), the leading cause of hospital admissions for gastrointestinal disorders. It is becoming increasingly clear that damage-associated molecular pattern molecules (DAMPs) play an important role in the pathogenesis of AP by linking local tissue damage to systemic inflammation syndrome. Endogenous DAMPs released from dead, dying or injured cells initiate and extend sterile inflammation via specific pattern recognition receptors. Inhibition of the release and activity of DAMPs (for example, high mobility group box 1, DNA, histones and adenosine triphosphate) provides significant protection against experimental AP . Moreover, increased serum levels of DAMPs in patients with AP correlate with disease severity. These findings provide novel insight into the mechanism, diagnosis and management of AP . DAMPs might be an attractive therapeutic target in AP.

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Release and activity of histone in diseases

Cited by 356 publications

References 82 publications

VEGF mitigates histone-induced pyroptosis in the remote liver injury associated with renal allograft ischemia–reperfusion injury in rats

VEGF mitigates histone-induced pyroptosis in the remote liver injury associated with renal allograft ischemia–reperfusion injury in rats

Role for Neutrophil Extracellular Traps (NETs) and Platelet Aggregation in Early Sepsis-induced Hepatic Dysfunction

Cell Death and DAMPs in Acute Pancreatitis

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