High Concentrations of TNF-α Induce Cell Death during Interactions between Human Umbilical Cord Mesenchymal Stem Cells and Peripheral Blood Mononuclear Cells

Li, Xue; Du, Weiting; Xia, Feng; Feng, Xiaoming; Bayard, Françis; Han, Zhongchao

doi:10.1371/journal.pone.0128647

Cited by 20 publications

(13 citation statements)

References 23 publications

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“…BAY 11-7082 is a specific pharmacologic NF-κB inhibitor with obvious cytotoxicity, which leads to increasing cell death as the concentration increases [87]. Some studies have shown that BAY 11-7082 impairs alveolar epithelial barrier function and causes unavoidable toxicity in cells and cultured brain tissue [88,89]. In the application of BAY 11-7085 system, toxic reactions were detected, so the local application of NF-κB inhibitor was paid more attention by many scholars.…”

Section: Therapeutic Prospects Of Targeting Inflammasomes In Renal DImentioning

confidence: 99%

Research Progress on the Role of Inflammasomes in Kidney Disease

Chi

Geng

Liu

et al. 2020

Mediators of Inflammation

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Inflammasomes are multimeric complexes composed of cytoplasmic sensors, apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC or PYCARD), and procaspase-1 and play roles in regulating caspase-dependent inflammation and cell death. Inflammasomes are assembled by sensing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) and initiate inflammatory responses by activating caspase-1. Activated caspase-1 promotes the release of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18 and eventually induces pyroptosis. Inflammasomes are closely related to kidney diseases. In particular, the NLRP3 (NACHT, LRR, and PYD domain-containing protein 3) inflammasome has been shown to cause acute and chronic kidney diseases by regulating canonical and noncanonical mechanisms of inflammation. Small-molecule inhibitors that target NLRP3 and other components of the inflammasome are potential options for the treatment of kidney-related diseases such as diabetic nephropathy. This article will focus on the research progress on inflammasomes and the key pathogenic roles of inflammasomes in the development and progression of kidney diseases and explore the potential of this intracellular inflammation to further prevent or block the development of the kidney disease.

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Section: Therapeutic Prospects Of Targeting Inflammasomes In Renal DImentioning

confidence: 99%

Research Progress on the Role of Inflammasomes in Kidney Disease

Chi

Geng

Liu

et al. 2020

Mediators of Inflammation

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“…Some previous studies reported that dexmedetomidine could inhibit the infl ammatory reaction by blocking the cascade reaction (16)(17)(18). In those studies, dexmedetomidine was shown to improve infl ammation by depressing the expression of IL-1β, and TNF-α which promote cell apoptosis (19,20). We supposed that dexmedetomidine might have direct effects on decreasing the cell apoptosis.…”

Section: Discussionmentioning

confidence: 84%

Dexmedetomidine protected COPD-induced lung injury by regulating miRNA-146a

Li¹,

Ouyang²,

Liu³

et al. 2016

BLL

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OBJECTIVE: To study the mechanism of protection provided by dexmedetomidine against COPD-induced lung injury. METHODS: COPD rat model was determined by measuring lung function, and comparing HE staining between two different groups. We got the lung tissue and cells from the control and COPD groups. The cells were divided into three groups: control group, and blank and drug groups that were from the COPD rats. Cell apoptosis, relative gene expression and TNF-α and IL-1β from nutrient solution were measured. Chronic obstructive pulmonary disease (COPD) is a kind of main damage located in airways and lung tissue, causing systemic disease progressively affecting other tissues and organs The symptoms are not reversible. Clinical research shows that the incidence of hospitalized patients with chronic pulmonary disease gradually increases (1). In 2040, COPD will become the world's most endangering disease (2, 3). COPD pathogenesis is not yet entirely clear, but the current study showed that the main causes of COPD include protease/anti-protease imbalance, oxidant/antioxidant imbalance stress (4-7), infl ammatory/anti-infl ammatory response imbalance (8), mechanical stretch injury (9), etc. Clinical treatment is often used for the purpose of mechanical ventilation after induction of anesthesia. Dexmedetomidine is a highly selective α2-adrenergic receptor agonist (10); it not only can effectively calm, but also has some anti-infl ammatory effect (11). However, the mechanism of dexmedetomidine protection against COPD is unclear. The objective of the present study is to explain the latter mechanism. Material and method Animals and cigarette smoke exposureIn our study, we used 6-week-old SD rats at body weight 110±20 g from the animal center, Nanfang Hospital of Southern Medical University. Before the experiment, the rats were accommodated for seven days. All procedures were in compliance with the institutional and national guidelines for the care and use of laboratory animals. The Study Protocol was approved by The Institutional Animal Care and Use Committee, Hebei Medical University. Rats were randomized into two groups: Control Group (n = 8) and Smoking Group (n = 16). The rats in smoking group were exposed to cigarette smoke in a smoking device manufactured by Shijiazhuang Jinyang Science and Technology Inc. (model: JY-01, Shijiazhuang, Hebei, China). Briefl y, 20 cigarettes were burnt continuously and blown into a box together with oxygen, while the whole bodies of animals were exposed to the cigarette smoke in the box. Animals were exposed to cigarette smoke for one hour each time, twice a day, 5 days a week for 16 weeks. After 16 weeks, the rats were analyzed for relative index of COPD including tidal volume (TV), peak expiratory fl ow (PEF), 50 % exhaled tidal volume during expiratory fl ow rate (EF50), forced expiratory volume in 0.3 seconds (FEV0.3) and FEV0.3/ forced vital capacity (FVC). Tissues and cellThe rats were sacrifi ced by femoral artery bleeding. Lung tissue was extracted and a proportion was ...

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“…Several studies have detected increased levels of TGF-α together with other cytokines in the mesenchymal stem cells derived from the umbilical cord in comparison with the cells derived from bone marrow suggesting their immunosuppressive properties [6,20]. TGF-α seemingly is an important growth factor for extraembryonic tissue development.…”

Section: Discussionmentioning

confidence: 99%