Tumor necrosis factor-alpha and interferon-gamma induce inflammasome-mediated corneal endothelial cell death

Gómez, Alejandro Raúl Gratacós; Serrano, Andres; Salero, Enrique; Tovar, Arianna; Amescua, Guillermo; Keane, Robert W.; Vaccari, Juan Pablo de Rivero; Sabater, Alfonso L.

doi:10.1016/j.exer.2021.108574

Cited by 29 publications

(17 citation statements)

References 62 publications

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“…Similarly, in macrophages and neurotrophils, NLR-family CARD-containing protein 4 (NLRC4) is reported to activate caspase-1 and trigger pyroptosis 44 . Meanwhile, after injuries, Neuronal apoptosis induced by ischaemia-reperfusion is associated with the neuroinflammation 45 , while oxidative stress induced by the injuries could stimulate the neuroinflammatory cascades, including activations of NLRP3 inflammasome and secretion of inflammatory cytokines, IL-1β, IL-18, TNF-α and IL-6 46 . Pro-inflammatory cytokines may further exacerbate neuronal apoptosis resulting in behavioural deficits 47 , 48 .…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective mechanism of lithium after ischaemic stroke

Chen

Zhang

et al. 2022

Commun Biol

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Stroke causes degeneration and death of neurones leading to the loss of motor function and frequent occurrence of cognitive impairment and depression. Lithium (Li+), the archetypal mood stabiliser, is neuroprotective in animal models of stroke, albeit underlying mechanisms remain unknown. We discover that Li+ inhibits activation of nucleotide-binding oligomerisation domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasomes in the middle cerebral artery occlusion (MCAO) stroke model in mice. This action of Li+ is mediated by two signalling pathways of AKT/GSK3β/β-catenin and AKT/FoxO3a/β-catenin which converge in suppressing the production of reactive oxygen species (ROS). Using immunocytochemstry, MRI imaging, and cell sorting with subsequent mRNA and protein quantification, we demonstrate that Li+ decreases the infarct volume, improves motor function, and alleviates associated cognitive and depressive impairments. In conclusion, this study reveals molecular mechanisms of Li+ neuroprotection during brain ischaemia, thus providing the theoretical background to extend clinical applications of Li+ for treatment of ischemic stroke.

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Section: Discussionmentioning

confidence: 99%

The neuroprotective mechanism of lithium after ischaemic stroke

Chen

Zhang

et al. 2022

Commun Biol

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“…Loss of corneal endothelial cells resulted in corneal edema and vision loss in endothelial keratopathy, such as pseudophakic bullous keratopathy, diabetic corneal endothelial keratopathy, and Fuchs' endothelial corneal dystrophy [ 75 ]. Corneal endothelial cell pyroptosis participates in diabetic corneal endothelial keratopathy [ 51 ] and pseudophakic bullous keratopathy [ 52 ].…”

Section: Relevance Of Pyroptosis In Corneal Diseasesmentioning

confidence: 99%

“…Pseudophakic bullous keratopathy is caused by injuries to the corneal endothelial cell, including surgical mechanical trauma, intraocular infusions, and drug injection. In human corneal endothelial cells, exposure to tumor necrosis factor- α (TNF- α ) and interferon- γ activated inflammasome and elevated oxidative stress, resulting in pyroptosis-induced cell loss [ 75 ]. Endothelial cell pyroptosis promotes inflammation and decreases the density of corneal endothelial cells, and these effects can be inhibited by Ac-YVAD-CMK [ 75 ].…”

Section: Relevance Of Pyroptosis In Corneal Diseasesmentioning

confidence: 99%

Roles and Mechanisms of Regulated Necrosis in Corneal Diseases: Progress and Perspectives

Lin

Chen

Cissé

et al. 2022

Journal of Ophthalmology

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Regulated necrosis is defined as cell death characterized by loss of the cell membrane integrity and release of the cytoplasmic content. It contributes to the development and progression of some diseases, including ischemic stroke injury, liver diseases, hypertension, and cancer. Various forms of regulated necrosis, particularly pyroptosis, necroptosis, and ferroptosis, have been implicated in the pathogenesis of corneal disease. Regulated necrosis of corneal cells enhances inflammatory reactions in the adjacent corneal tissues, leading to recurrence and aggravation of corneal disease. In this review, we summarize the molecular mechanisms of pyroptosis, necroptosis, and ferroptosis in corneal diseases and discuss the roles of regulated necrosis in inflammation regulation, tissue repair, and corneal disease outcomes.

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“…The data suggest that HPW can ameliorate the downregulated expression caused by 5-FU administration, which may be one of the molecular mechanisms by which HPW can improve inflammation in the small intestinal mucosa. In addition, other studies have demonstrated that TNF-α may initiate the infiltration of inflammatory cells into the intestine by decreasing the expression of occludin, leading to structural changes in tight junctions [ 48 ]. COX-2 destroys the collagen subepithelial matrix and epithelial basement membrane by activating matrix metalloproteinases, which further damages the small intestinal mucosal barrier [ 49 ].…”

Section: Discussionmentioning

confidence: 99%

Protective effect of homogeneous polysaccharides of Wuguchong (HPW) on intestinal mucositis induced by 5-fluorouracil in mice

et al. 2022

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Background In hospitalized patients, drug side effects usually trigger intestinal mucositis (IM), which in turn damages intestinal absorption and reduces the efficacy of treatment. It has been discovered that natural polysaccharides can relieve IM. In this study, we extracted and purified homogenous polysaccharides of Wuguchong (HPW), a traditional Chinese medicine, and explored the protective effect of HPW on 5-fluorouracil (5-FU)-induced IM. Methods and results First, we identified the physical and chemical properties of the extracted homogeneous polysaccharides. The molecular weight of HPW was 616 kDa, and it was composed of 14 monosaccharides. Then, a model of small IM induced by 5-FU (50 mg/kg) was established in mice to explore the effect and mechanism of HPW. The results showed that HPW effectively increased histological indicators such as villus height, crypt depth and goblet cell count. Moreover, HPW relieved intestinal barrier indicators such as D-Lac and diamine oxidase (DAO). Subsequently, western blotting was used to measure the expression of Claudin-1, Occludin, proliferating cell nuclear antigen, and inflammatory proteins such as NF-κB (P65), tumour necrosis factor-α (TNF-α), and COX-2. The results also indicated that HPW could reduce inflammation and protect the barrier at the molecular level. Finally, we investigated the influence of HPW on the levels of short-chain fatty acids, a metabolite of intestinal flora, in the faeces of mice. Conclusions HPW, which is a bioactive polysaccharide derived from insects, has protective effects on the intestinal mucosa, can relieve intestinal inflammation caused by drug side effects, and deserves further development and research.

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Tumor necrosis factor-alpha and interferon-gamma induce inflammasome-mediated corneal endothelial cell death

Cited by 29 publications

References 62 publications

The neuroprotective mechanism of lithium after ischaemic stroke

The neuroprotective mechanism of lithium after ischaemic stroke

Roles and Mechanisms of Regulated Necrosis in Corneal Diseases: Progress and Perspectives

Protective effect of homogeneous polysaccharides of Wuguchong (HPW) on intestinal mucositis induced by 5-fluorouracil in mice

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