Contributions of High Mobility Group Box Protein in Experimental and Clinical Acute Lung Injury

Ueno, Hiroshi; Matsuda, Tomoyuki; Hashimoto, Satoru; Amaya, Fumimasa; Kitamura, Yoshihiro; Tanaka, Masaki; Kobayashi, Atsuko; Maruyama, Ikuro; Yamada, Shingo; Hasegawa, Naoki; Soejima, Junko; Koh, Hidefumi; Ishizaka, Akitoshi

doi:10.1164/rccm.200402-188oc

Cited by 318 publications

(273 citation statements)

References 25 publications

Supporting

Mentioning

254

Contrasting

Order By: Relevance

“…HMGB1 mRNA and protein were also produced by macrophages and cardiomyocytes followed by increased NFkappaB binding activity with consecutively sustained TNFand IL-6 expression [20]. HMGB1 activates HUVECs (human umbilic vein endothelial cells) to produce multiple inflammatory cytokines, such as IFN-, IL-6 and IL-8 [21].…”

Section: Disscussionmentioning

confidence: 99%

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Luo

Xie

Gong

et al. 2011

Archives of Oral Biology

View full text Add to dashboard Cite

High mobility group chromosomal protein B1 (HMGB1) and N2 (HMGN2), two members of High mobility group (HMG) family, play important role in inflammation. The purposes of this study were to investigate the expression of HMGB1 and HMGN2 in periodontistis.The expression of HMGB1 and HMGN2 mRNA in gingival tissues and gingival crevicular fluid (GCF) in chronic periodontitis (CP), generalized aggressive periodontitis (G-AgP) patients and healthy subjects was detected by real-time PCR. The protein level of HMGB1 and HMGN2 in peri-implant crevicular fluid (PICF), peri-implant crevicular fluid of peri-implantitis (PI-PICF) and normal patients was determined by Western blotting. Furthermore, IL-1 , IL-6, IL-8, TNF-and HMGB1 levels in GCF, PI-PICF and healthy-PICF samples from different groups were determined by ELISA.HMGN2 expression was increased in inflamed gingival tissues and GCF from CP and G-ApG groups compared to control group. HMGB1 expression was the highest in the gingival tissues and GCF from CP patients and was accompanied by increased concentrations of IL-1 , IL-6, IL-8 proinflammaory cytokines.To our knowledge, this is the first study reporting that the expression of HMGB1 and HMGN2 was increased in the gingival tissues and GCF in CP and G-AgP and the PICF in PICF. Our data suggest that HMGB1 may be a potential target for the therapy of periodontitis and PI.

show abstract

Section: Disscussionmentioning

confidence: 99%

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Luo

Xie

Gong

et al. 2011

Archives of Oral Biology

View full text Add to dashboard Cite

show abstract

“…HMGB-1 and RAGE are known to be causally involved in a variety of pathophysiological processes, such as rheumatoid arthritis, acute lung injury, disseminated intravascular coagulation, Alzheimer disease, tumorigenesis, abnormalities associated with diabetes, and impaired wound healing [8,[17][18][19][20][21][22]. Although HMGB-1 is regarded as a trigger of these immune/inflammatory disorders mediated via RAGE and TLR and also affects immunological abnormalities [5,6,9,12,23], correlation of serum…”

Section: Serum Levels Of Hmgb-1 and Srage In Sscmentioning

confidence: 99%

Clinical Significance of Serum HMGB-1 and sRAGE Levels in Systemic Sclerosis: Association with Disease Severity

et al. 2008

View full text Add to dashboard Cite

The high mobility group box 1 protein (HMGB-1)/adcanced glycation end products (RAGE) system is recently shown to play an important part in immune/inflammatory disorders. However, the association of this system in systemic sclerosis (SSc) remains unknown. To determine clinical association of serum levels of HMGB-1 and soluble RAGE (sRAGE) in patients with SSc, sera from 70 patients with SSc and 25 healthy controls were examined by enzyme-linked immunosorbent assay. Sera from Tight-skin mice and bleomycin-induced scleroderma mice, animal models for SSc, were also examined. Skin HMGB-1 and RAGE expression was assessed by immunohistochemistry. Serum HMGB-1 and sRAGE levels in SSc were higher than those in controls. Similarly, HMGB-1 and sRAGE levels in animal SSc models were higher than those in control mice. SSc patients with elevated HMGB-1 and sRAGE levels had more frequent involvement of several organs and immunological abnormalities compared to those with normal levels. Furthermore, HMGB-1 and sRAGE levels correlated positively with modified Rodnan total skin thickness score and negatively with pulmonary function test. HMGB-1 and sRAGE expression in the sclerotic skin was more intense than normal skin. These results suggest that elevated serum HMGB-1 and sRAGE levels are associated with the disease severity and

show abstract

“…HMGB1 amplifies and extends the inflammatory response by inducing the release of other proinflammatory cytokines from many cell types, including activated macrophages and neutrophil [126]. Elevated levels of HMGB1 are present in the plasma and lung epithelial lining fluids of patients with acute lung injury and in mice exhibiting lung injury-induced by LPS instillation [127]. Intratracheal administration of HMGB1 to mice causes acute lung injury as manifested by neutrophil accumulation, lung edema, and increased pulmonary levels of cytokines, including TNF-α, IL-1β, and macrophage inflammatory protein-2 (MIP-2) and macrophage migration inhibitory factor (MIF) [128,129].…”

Section: Proinflammatory Responses In Hyperoxic Lung Injurymentioning

confidence: 99%

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells☆

Zaher

Miller

Morrow

et al. 2007

Free Radical Biology and Medicine

119

View full text Add to dashboard Cite

Mechanical ventilation with hyperoxia is necessary to treat critically ill patients. However, prolonged exposure to hyperoxia leads to the generation of excessive reactive oxygen species (ROS), which can cause acute inflammatory lung injury. One of the major effects of hyperoxia is the injury and death of pulmonary epithelium, which is accompanied by increased levels of pulmonary proinflammatory cytokines and excessive leukocyte infiltration. A thorough understanding of the signaling pathways leading to pulmonary epithelial cell injury/death may provide some insights into the pathogenesis of hyperoxia-induced acute inflammatory lung injury. This review focuses on epithelial responses to hyperoxia and some of the major factors regulating pathways to epithelial cell injury/death, and proinflammatory responses upon exposure to hyperoxia. We discuss in detail some of the most interesting players, such as, NF-κB, that can modulate both proinflammatory responses and cell injury/death of lung epithelial cells. A better appreciation for the functions of these factors will no doubt help us to delineate the pathways to hyperoxic cell death and proinflammatory responses.

show abstract

Contributions of High Mobility Group Box Protein in Experimental and Clinical Acute Lung Injury

Cited by 318 publications

References 25 publications

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Clinical Significance of Serum HMGB-1 and sRAGE Levels in Systemic Sclerosis: Association with Disease Severity

Hyperoxia-induced signal transduction pathways in pulmonary epithelial cells☆

Contact Info

Product

Resources

About