Caspase-1 activation and mature interleukin-1β release are uncoupled events in monocytes

Galliher-Beckley, Amy; Lan, Liqiong; Aono, Shelly; Wang, Lei; Shi, Jishu

doi:10.4331/wjbc.v4.i2.30

Cited by 24 publications

(12 citation statements)

References 23 publications

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“…In contrast, stimulating the cells with exogenous peroxynitrite as a model of oxidative stress resulted in a higher surge of IL-1b release that was independent of TXNIP inhibition, although it was not able to induce significant changes in its intracellular cleavage/maturation, suggesting accelerated activation and trafficking of IL-1b. These findings lend further support to previous evidence that the process of caspase-1 activation/processing of pro-IL-1b by caspase-1 and the release of mature IL-1b from human monocytes are distinct and separable events (38). TXNIP has been shown to shuffle between different cellular compartments, including the nucleus, mitochondria (75), and plasma membrane (110).…”

Section: Nlrp3-inflammasome Activation In Pre-drsupporting

confidence: 88%

Role of Inflammasome Activation in the Pathophysiology of Vascular Diseases of the Neurovascular Unit

Mohamed

Ishrat²,

Fagan³

et al. 2015

Antioxidants & Redox Signaling

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Section: Nlrp3-inflammasome Activation In Pre-drsupporting

confidence: 88%

Role of Inflammasome Activation in the Pathophysiology of Vascular Diseases of the Neurovascular Unit

Mohamed

Ishrat²,

Fagan³

et al. 2015

Antioxidants & Redox Signaling

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“…This data indicate that, while TXNIP is required for palmitate-induced NLRP3 inflammasome activation and IL-1β maturation in HRE cells, it does not facilitate the maximum IL-1β release. Recent evidence suggests that caspase-1 activation/processing of pro-IL-1β by caspase-1 and the release of mature IL-1β from human monocytes are distinct and separable events [47]. TXNIP has been shown to shuffle between different cellular compartments, including the nucleus, mitochondria [48] and plasma membrane [49].…”

Section: Discussionmentioning

confidence: 99%

Thioredoxin-interacting protein is required for endothelial NLRP3 inflammasome activation and cell death in a rat model of high-fat diet

et al. 2013

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Aims/hypothesis Obesity and hypertension, known pro-inflammatory states, are identified determinants for increased retinal microvascular abnormalities. However, the molecular link between inflammation and microvascular degeneration remains elusive. Thioredoxin-interacting protein (TXNIP) is recognised as an activator of the NOD-like receptor pyrin domain containing-3 (NLRP3) inflammasome. This study aims to examine TXNIP expression and elucidate its role in endothelial inflammasome activation and retinal lesions. Methods Spontaneously hypertensive (SHR) and control Wistar (W) rats were compared with groups fed a high-fat diet (HFD) (W+F and SHR+F) for 8–10 weeks. Results Compared with W controls, HFD alone or in combination with hypertension significantly induced formation of acellular capillaries, a hallmark of retinal ischaemic lesions. These effects were accompanied by significant increases in lipid peroxidation, nitrotyrosine and expression of TXNIP, nuclear factor κB, TNF-α and IL-1β. HFD significantly increased interaction of TXNIP–NLRP3 and expression of cleaved caspase-1 and cleaved IL-1β. Immunolocalisation studies identified TXNIP expression within astrocytes and Müller cells surrounding retinal endothelial cells. To model HFD in vitro, human retinal endothelial (HRE) cells were stimulated with 400 μmol/l palmitate coupled to BSA (Pal-BSA). Pal-BSA triggered expression of TXNIP and its interaction with NLRP3, resulting in activation of caspase-1 and IL-1β in HRE cells. Silencing Txnip expression in HRE cells abolished Pal-BSA-mediated cleaved IL-1β release into medium and cell death, evident by decreases in cleaved caspase-3 expression and the proportion of live to dead cells. Conclusions/interpretation These findings provide the first evidence for enhanced TXNIP expression in hypertension and HFD-induced retinal oxidative/inflammatory response and suggest that TXNIP is required for HFD-mediated activation of the NLRP3 inflammasome and the release of IL-1β in endothelial cells.

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“…Cellular isolation is harsh and incurred stress lead to the release of endogenous danger signals (danger-activated molecular patterns) and activation of purinergic receptors, all of which contribute to inflammasome activation and consequent IL-1β production (so-called sterile inflammation) [25,26]. For example, if cells are stimulated with LPS then mature IL-1β is principally observed in freshly isolated monocytes rather than their 1-day rested counterparts [27][28][29]. Therefore, we first tested whether this also applied to primary human blood cells stimulated with the freshly formed apatitic nanoparticles.…”

Section: Effect Of Resting Of Cells and Tcm Filtrationmentioning

confidence: 98%

Artefactual Nanoparticle Activation of the Inflammasome Platform: in Vitro Evidence with a Nano-Formed Calcium Phosphate

Pele

Haas

Hewitt

et al. 2014

Nanomedicine (Lond.)

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Caspase-1 activation and mature interleukin-1β release are uncoupled events in monocytes

Abstract: These data suggest that caspase-1 activation/processing of pro-IL-1β by caspase-1 and the release of mature IL-1β from human monocytes are distinct and separable events.

Cited by 24 publications

References 23 publications

Role of Inflammasome Activation in the Pathophysiology of Vascular Diseases of the Neurovascular Unit

Role of Inflammasome Activation in the Pathophysiology of Vascular Diseases of the Neurovascular Unit

Thioredoxin-interacting protein is required for endothelial NLRP3 inflammasome activation and cell death in a rat model of high-fat diet

Artefactual Nanoparticle Activation of the Inflammasome Platform: in Vitro Evidence with a Nano-Formed Calcium Phosphate

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