Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis

Guo-qian, Chen; Li, Jianhua; Qiang, Xiaoling; Czura, Christopher J.; Ochani, Mahendar; Ochani, Kanta; Ulloa, Luis; Yang, Huan; Tracey, Kevin J.; Wang, Ping; Sama, Andrew E.; Wang, Haichao

doi:10.1194/jlr.c400018-jlr200

Cited by 108 publications

(98 citation statements)

References 19 publications

(52 reference statements)

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“…89,90 LPC has been shown to both increase production of proinflammatory cytokines, 69 and have anti-inflammatory effects such as inhibiting high-mobility group protein B1 (HMGB1) secretion(16 h post-treatment with LPC). 91 These effects are dependent on different receptors as well as cell types, but not yet fully understood. LPC can also act as an indirect eat-me signal by promoting the LPC-dependent binding of IgM to apoptotic, 92 late apoptotic 93,94 and necrotic cells, 95 ultimately leading to clearance.…”

Section: Steps Involved In Clearancementioning

confidence: 99%

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

2016

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The turnover and clearance of cells is an essential process that is part of many physiological and pathological processes. Improper or deficient clearance of apoptotic cells can lead to excessive inflammation and autoimmune disease. The steps involved in cell clearance include: migration of the phagocyte toward the proximity of the dying cells, specific recognition and internalization of the dying cell, and degradation of the corpse. The ability of phagocytes to recognize and react to dying cells to perform efficient and immunologically silent engulfment has been well-characterized in vitro and in vivo. However, how apoptotic cells themselves initiate the corpse removal and also influence the cells within the neighboring environment during clearance was less understood. Recent exciting observations suggest that apoptotic cells can attract phagocytes through the regulated release of 'find-me' signals. More recent studies also suggest that these find-me signals can have additional roles outside of phagocyte attraction to help orchestrate engulfment. This review will discuss our current understanding of the different find-me signals released by apoptotic cells, how they may be relevant in vivo, and their additional roles in facilitating engulfment.

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Section: Steps Involved In Clearancementioning

confidence: 99%

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

2016

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“…It is constitutively expressed in quiescent cells, and a large 'pool' of preformed HMGB1 is stored in the nucleus [2] as a result of the presence of two lysine-rich nuclear localization sequences [3]. HMGB1 is among the most evolutionarily conserved proteins in eukaryotes: it shares 100% identity in amino acid sequence between mouse and rat, and a 99% amino acid identity between rodent and human [1••].…”

Section: Introductionmentioning

confidence: 99%

Role of HMGB1 in cardiovascular diseases

Sama

Wang

2006

Current Opinion in Pharmacology

107

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A nuclear protein, high mobility group box 1 (HMGB1), is released passively by necrotic cells, and actively by macrophages/monocytes in response to exogenous and endogenous inflammatory stimuli. After binding to the receptor for advanced glycation end products (RAGE) or toll-like receptor 4 (TLR4), HMGB1 activates vascular endothelial cells and macrophages/monocytes to express proinflammatory cytokines, chemokines and adhesion molecules. Pharmacological suppression of its activities or release is protective against lethal endotoxemia and sepsis, establishing HMGB1 as a critical mediator of lethal systemic inflammation. In light of the pathogenic role of inflammation in cardiovascular diseases, we propose that HMGB1, a proinflammatory cytokine derived from both injured endothelium and activated macrophages/monocytes, could contribute to the progression of atherosclerosis and other cardiovascular diseases.

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“…Indeed, ethyl pyruvate, stearoyl lysophosphatidylcholine and nicotine have already been shown to be efficacious in ameliorating experimental sepsis by preventing HMGB1 release (Ulloa et al, 2003;Wang et al, 2004;Chen et al, 2005). However, the mechanism by which they do so is unclear and these compounds are likely also to affect numerous other cell processes.…”

Section: Resultsmentioning

confidence: 99%

Targeting DAMP Activation of Toll-Like Receptors: Novel Pathways to Treat Rheumatoid Arthritis?

Page¹,

Midwood²

2012

Rheumatoid Arthritis - Treatment

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Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsis

Cited by 108 publications

References 19 publications

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Do not let death do us part: ‘find-me’ signals in communication between dying cells and the phagocytes

Role of HMGB1 in cardiovascular diseases

Targeting DAMP Activation of Toll-Like Receptors: Novel Pathways to Treat Rheumatoid Arthritis?

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