Peroxynitrite induces HMGB1 release by cardiac cells in vitro and HMGB1 upregulation in the infarcted myocardium in vivo

Loukili, Noureddine; Rosenblatt‐Velin, Nathalie; Li, Jianhui; Clerc, S; Pacher, Pál; Feihl, François; Waeber, Bernard; Liaudet, Lucas

doi:10.1093/cvr/cvq373

Cited by 71 publications

(66 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Loukili, et al showed that the expression of HMGB1 in hearts increased significantly after 1 hour of reperfusion, further increased after 2 hours of reperfusion, and then no further increase was observed thereafter. 13) As we showed in this study, P.g. infection significantly elevated serum HMGB1 levels on day 5, but not on day 14.…”

Section: Discussionsupporting

confidence: 64%

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

et al. 2017

View full text Add to dashboard Cite

SummaryHigh mobility group box 1 (HMGB1) is a nuclear protein released from necrotic cells, inducing inflammatory responses. Epidemiological studies suggested a possible association between periodontitis and cardiovascular diseases (CVDs). Due to tissue damage and necrosis of cardiac cells following myocardial infarction (MI), HMGB1 is released, activating an inflammatory reaction. However, it remains unclear whether periodontitis is also involved in myocardial damage. The purpose of this study was to determine the effect of the periodontal pathogen Porphyromonas gingivalis (P.g.) after MI in mice.C57BL/6J wild type mice in post-MI were inoculated with P.g. in the infected group (P.g.-inoculated MI group) and with phosphate buffer saline (PBS) in the control group (PBS-injected MI group). Plasma samples and twelve tissue samples from mice hearts after MI were obtained. We determined the expression of HMGB1 by ELISA and immunohistochemistry.The level of HMGB1 protein in the P.g.-inoculated MI group was significantly higher than in the PBSinjected MI group on day 5, but not on day 14. Immunohistochemistry analysis revealed that HMGB1 was mainly expressed in cardiomyocytes, immune cells, and vascular endothelial cells in the PBS-injected MI group, while HMGB1 was seen broadly in degenerated cardiomyocytes, extracellular fields, immune cells, and vascular endothelial cells in the P.g.-inoculated MI group. A significant increase in the number of HMGB1 positive cells was observed in the P.g.-inoculated MI group compared to the PBS-injected MI group.Infection with P.g. after MI enhanced myocardial HMGB1 expression. There is a possible relationship between periodontitis and post-infarction myocardial inflammation through HMGB-1.(Int Heart J 2017; 58: 762-768)

show abstract

Section: Discussionsupporting

confidence: 64%

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

et al. 2017

View full text Add to dashboard Cite

show abstract

“…HMGB1 also forms various complexes with many different molecules in the extracellular milieu, promoting additional pro-inflammatory activities through interaction with TLR2, TLR3, TLR9, and the IL-1 receptor (Bianchi, 2009;Janko et al, 2013). HMGB1 plays significant roles in the pathophysiology of sterile inflammation (Andersson and Tracey, 2011) associated with diverse acute and chronic conditions, including myocardial infarction (Loukili et al, 2011), hepatic ischemia (Tsung et al, 2005), stroke (Schulze et al, 2013), circulatory shock and trauma (Andersson and Tracey, 2011), diabetes (Nogueira-Machado et al, 2011), cancer (Krysko et al, 2012), and arthritis (Harris et al, 2012), and it also acts as a key pro-inflammatory cytokine involved in the pathogenesis of sepsis (Yang et al, 2004). Thus, HMGB1 emerges as a central acting mediator at the intersection between sterile and infectious inflammation (Andersson and Tracey, 2011).…”

Section: Role Of Oxidative Stress In Inflammationmentioning

confidence: 99%

“…In a study using isolated cardiomyocytes in vitro, we reported that exposure of the cells to toxic concentrations of peroxynitrite induced necrotic cell death and was associated with the release of copious amounts of HMGB1 (Loukili et al, 2011). Similarly, Tang et al (2007Tang et al ( , 2011 reported that treatment of various mouse and human cell lines with H 2 O 2 promoted significant extracellular HMGB1 release, whereas Tsung et al (2007) showed that oxidants promoted the active release of HMGB1 by cultured hepatocytes through calmodulin-dependent kinase signaling.…”

Section: Role Of Oxidative Stress In Inflammationmentioning

confidence: 99%

The role of oxidative stress during inflammatory processes

Lugrin¹,

Rosenblatt‐Velin

Parapanov³

et al. 2013

Biological Chemistry

557

393

View full text Add to dashboard Cite

Abstract:The production of various reactive oxidant species in excess of endogenous antioxidant defense mechanisms promotes the development of a state of oxidative stress, with significant biological consequences. In recent years, evidence has emerged that oxidative stress plays a crucial role in the development and perpetuation of inflammation, and thus contributes to the pathophysiology of a number of debilitating illnesses, such as cardiovascular diseases, diabetes, cancer, or neurodegenerative processes. Oxidants affect all stages of the inflammatory response, including the release by damaged tissues of molecules acting as endogenous danger signals, their sensing by innate immune receptors from the Toll-like (TLRs) and the NOD-like (NLRs) families, and the activation of signaling pathways initiating the adaptive cellular response to such signals. In this article, after summarizing the basic aspects of redox biology and inflammation, we review in detail the current knowledge on the fundamental connections between oxidative stress and inflammatory processes, with a special emphasis on the danger molecule highmobility group box-1, the TLRs, the NLRP-3 receptor, and the inflammasome, as well as the transcription factor nuclear factor-κB.

show abstract

“…Tsung et al (14) further demonstrated that the release of HMGB1 from cultured hepatocytes was also found to be an active process regulated by ROS. Recently, Loukili et al (15) showed that peroxynitrite, a potent cytotoxic oxidant, was involved in the release of HMGB1 in cardiac cells. Hence, inhibiting ROS may cause suppression of HMGB1 expression.…”

Section: Discussionmentioning

confidence: 99%

Geranylgeranylacetone protects against myocardial ischemia and reperfusion injury by inhibiting high-mobility group box 1 protein in rats

Wang

Min

et al. 2011

Mol Med Report

View full text Add to dashboard Cite

Abstract. The high mobility group box 1 (HMGB1) protein plays an important role in myocardial ischemia and reperfusion (I/R) injury. Geranylgeranylacetone (GGA), a heat shock protein 72 inducer, has been reported to reduce myocardial I/R injury. The aim of this study was to investigate the cardioprotective mechanism of GGA during myocardial I/R injury in rats. Anesthetized male rats were treated once with GGA (200 mg/ kg, p.o.) 24 h before ischemia, and subjected to ischemia for 30 min, followed by reperfusion for 4 h. Lactate dehydrogenase (LDH), creatine kinase (CK), malondialdehyde (MDA), superoxide dismutase (SOD) activity and infarct size were measured. HMGB1 expression was assessed by immunoblotting. The results showed that pre-treatment with GGA (200 mg/kg) significantly reduced the infarct size and the levels of LDH and CK after 4 h of reperfusion (all P<0.05). GGA also significantly inhibited the increase in MDA levels and the decrease in SOD levels (both P<0.05). Meanwhile, GGA considerably suppressed the expression of HMGB1 induced by I/R. The present study suggests that GGA is capable of attenuating myocardial I/R injury by inhibiting HMGB1 expression.

show abstract

Peroxynitrite induces HMGB1 release by cardiac cells in vitro and HMGB1 upregulation in the infarcted myocardium in vivo

Abstract: These findings indicate that peroxynitrite represents a key mediator of HMGB1 overexpression and release by cardiac cells and provide a novel mechanism linking myocardial oxidative/nitrosative stress with post-infarction myocardial inflammation.

Cited by 71 publications

References 50 publications

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

<i>Porphyromonas Gingivalis</i> Elevated High-Mobility Group Box 1 Levels After Myocardial Infarction in Mice

The role of oxidative stress during inflammatory processes

Geranylgeranylacetone protects against myocardial ischemia and reperfusion injury by inhibiting high-mobility group box 1 protein in rats

Contact Info

Product

Resources

About