The Expression of HMGB1 on Microparticles Released during Cell Activation and Cell Death In Vitro and In Vivo

Pisetsky, David S.

doi:10.2119/molmed.2014.00014

Cited by 61 publications

(54 citation statements)

References 57 publications

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“…High-mobility group box 1 secretion has been observed to be through both active (from monocytic cells) and passive mechanisms (secondary to necrosis or apoptosis) (Gardella et al, 2002; Pisetsky, 2014; Scaffidi et al, 2002; Willingham et al, 2009). Increased cytotoxicity has been observed with MWCNT exposure in epithelial cells and AM (Beamer et al, 2013; Hamilton et al, 2012), however the pre-dominant form of MWCNT-induced cell death is conflicting, and likely depends upon particle physiochemical and surface properties.…”

Section: Discussionmentioning

confidence: 99%

“…High-mobility group box 1 (HMGB1) is a nuclear architectural protein that is secreted from injured/dead cells (Pisetsky, 2014; Scaffidi et al, 2002; Stros, 2010; Yang et al, 2010b), as well as actively secreted from cells of monocytic origin (Gardella et al, 2002). Secreted HMGB1 belongs to a large family of Danger Associated Molecular Patterns (DAMPs) ligands, and has been implicated as an activator of NF-κB in sterile inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Jessop

Holian

2014

Nanotoxicology

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Endotoxin is often used to activate NF-κB in vitro when assessing NLRP3 inflammasome activation by various exogenous particles including nanoparticles. However, the endogenous source of this signal 1 is unknown. High-mobility group box 1 (HMGB1) is known to play a critical role in acute lung injury, however the potential contribution of the alarmin HMGB1 to NLRP3 Inflammasome activation has not been determined in response to nanoparticles in vivo. In this study, the ability of multi-walled carbon nanotubes (MWCNT) to cause release of HMGB1 in vitro and in vivo, as well as the potential of HMGB1 to function as signal 1 in vitro and in vivo, was determined. HMGB1 activity in vivo was assessed by administration of HMGB1 neutralization antibodies following MWCNT exposure. Caspase-1−/− mice were utilized to elucidate the dependence of HMGB1 secretion on NLRP3 inflammasome activity. MWCNT exposure increased extracellular HMGB1 levels in primary alveolar macrophages from C57Bl/6 mice and C10 mouse epithelial cell culture supernatants, and in C57Bl/6 mouse lung lavage fluid. MWCNT-induced HMGB1 secretion was dependent upon caspase-1. HMGB1 increased MWCNT-induced IL-1β release from macrophages in vitro, and neutralization of extracellular HMGB1 reduced MWCNT-induced IL-1β secretion in vivo. HMGB1 neutralization was accompanied with overall decreased inflammation. In summary, this study suggests extracellular HMGB1 participates in NLRP3 inflammasome activity and regulates IL-1β associated sterile inflammation induced by MWCNT.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Jessop

Holian

2014

Nanotoxicology

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“…Composition and cell origin of MVs was done as described [35, 36]. Briefly, MVs were permeabilized with Fix/Perm buffer (Biolegend), incubated with Fc blocking buffer (Biolegend), and labeled using antibodies to HMGB1, GFAP (astrocytes), Na + /K + ATPase α3 (neurons), and CD11b (microglia).…”

Section: Methodsmentioning

confidence: 99%

Microglial-derived miRNA let-7 and HMGB1 contribute to ethanol-induced neurotoxicity via TLR7

Coleman

Zou

Crews

2017

J Neuroinflammation

185

198

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BackgroundToll-like receptor (TLR) signaling is emerging as an important component of neurodegeneration. TLR7 senses viral RNA and certain endogenous miRNAs to initiate innate immune responses leading to neurodegeneration. Alcoholism is associated with hippocampal degeneration, with preclinical studies linking ethanol-induced neurodegeneration with central innate immune induction and TLR activation. The endogenous miRNA let-7b binds TLR7 to cause neurodegeneration.MethodsTLR7 and other immune markers were assessed in postmortem human hippocampal tissue that was obtained from the New South Wales Tissue Bank. Rat hippocampal-entorhinal cortex (HEC) slice culture was used to assess specific effects of ethanol on TLR7, let-7b, and microvesicles.ResultsWe report here that hippocampal tissue from postmortem human alcoholic brains shows increased expression of TLR7 and increased microglial activation. Using HEC slice culture, we found that ethanol induces TLR7 and let-7b expression. Ethanol caused TLR7-associated neuroimmune gene induction and initiated the release let-7b in microvesicles (MVs), enhancing TLR7-mediated neurotoxicity. Further, ethanol increased let-7b binding to the danger signaling molecule high mobility group box-1 (HMGB1) in MVs, while reducing let-7 binding to classical chaperone protein argonaute (Ago2). Flow cytometric analysis of MVs from HEC media and analysis of MVs from brain cell culture lines found that microglia were the primary source of let-7b and HMGB1-containing MVs.ConclusionsOur results identify that ethanol induces neuroimmune pathology involving the release of let-7b/HMGB1 complexes in microglia-derived microvesicles. This contributes to hippocampal neurodegeneration and may play a role in the pathology of alcoholism.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0799-4) contains supplementary material, which is available to authorized users.

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“…HMGB1 is actively released from activated immune cells in response to injuries and infections. It can also be passively released from damaged/necrotic cells [7][8][9][10]. HMGB1 acts as an alarmin signal to alert, recruit, and activate immune cells in the extracellular space [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

HMGB1 regulates IL-33 expression in acute respiratory distress syndrome

Lin

Wang

et al. 2016

International Immunopharmacology

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The Expression of HMGB1 on Microparticles Released during Cell Activation and Cell Death In Vitro and In Vivo

Cited by 61 publications

References 57 publications

Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Extracellular HMGB1 regulates multi-walled carbon nanotube-induced inflammation in vivo

Microglial-derived miRNA let-7 and HMGB1 contribute to ethanol-induced neurotoxicity via TLR7

HMGB1 regulates IL-33 expression in acute respiratory distress syndrome

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