Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway

Yin, Yanlin; Zhou, Zhenhua; Liu, Weiwei; Chang, Qun; Sun, Guanqun; Dai, Yue

doi:10.1016/j.biocel.2017.01.001

Cited by 102 publications

(77 citation statements)

References 48 publications

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“…Previous research has indicated that high levels of ROS under multiple kinds of cellular stress, particularly those produced by mitochondria (mtROS), activates the NLRP3 inflammasome signal pathway (71)(72)(73)(74). In detail, high levels of ROS induce the ROS scavenging protein thioredoxin resolving from thioredoxin interacting/inhibiting protein (TXNIP), which then directly binds with NLRP3 proteins and modulates its assembly via oligomerization (75)(76)(77). Although several investigations have demonstrated that TXNIP is necessary for NLRP3 inflammasome assembly, a cell type-specific modulation of TXNIP occurs, which limits its mediation of inflammatory response ROS signaling pathway activation to particular cell types (78)(79)(80).…”

Section: Activation Of the Nlrp3 Inflammasome Pathway In Ischemic Strokementioning

confidence: 99%

Evidence and perspective for the role of the NLRP3 inflammasome signaling pathway in ischemic stroke and its therapeutic potential (Review)

Liu

Zhang

et al. 2018

Int J Mol Med

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Section: Activation Of the Nlrp3 Inflammasome Pathway In Ischemic Strokementioning

confidence: 99%

Evidence and perspective for the role of the NLRP3 inflammasome signaling pathway in ischemic stroke and its therapeutic potential (Review)

Liu

Zhang

et al. 2018

Int J Mol Med

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“…18. ROS have been reported to be key mediators in the activation of the NLRP3 inflammasome (19)(20)(21). Intracellular ROS generation was measured in response to leptin within RAW 264.7 cells.…”

Section: Leptin Promotes Il-18 Secretion In Raw 2647 Cellsmentioning

confidence: 99%

Leptin promotes IL-18 secretion by activating the NLRP3 inflammasome in RAW 264.7 cells

Liu

Han

et al. 2017

Molecular Medicine Reports

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Leptin is a cytokine‑like hormone secreted by adipocytes, which serves to control energy expenditure and metabolism. In addition, leptin may modulate the innate and adaptive immune responses. The innate immune cell sensor nucleotide‑binding oligomerization domain‑like receptor family pyrin domain‑containing 3 (NLRP3) inflammasome is mainly expressed in myeloid immune cells, including macrophages. The NLRP3 inflammasome serves a pivotal role in the development and maintenance of autoimmunity and inflammation. The expression levels of caspase‑1, apoptosis‑associated speck‑like protein containing a CARD, interleukin (IL)‑18, IL‑1β and leptin are significantly reduced in the white adipose tissue of nonsteroidal anti‑inflammatory drug‑activated gene‑1 transgenic mice. However, the association between leptin and the NLRP3 inflammasome has not yet to be determined. The aim of the present study, was to explore the role of leptin on NLRP3 inflammasome. In order to do this, IL‑1β and IL‑18 expression levels were investigated in RAW 264.7 cells after incubation with leptin of increasing doses by Elisa or reverse transcription‑quantitative polymerase chain reaction, and to assess whether IL‑1β and IL‑18 were affected after caspase‑1 activity being inhibited by an inhibitor or by silencing NLRP3 expression. The results of the present study demonstrated that leptin enhanced the mRNA and protein expression levels of IL‑18 in RAW 264.7 cells via activation of the NLRP3 inflammasome. This is achieved partly by enhancing the production of reactive oxygen species and K+ efflux. Therefore, leptin may be considered a novel activator and modulator of the NLRP3 inflammasome.

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“…With the exception of the ER and peroxisomes, mitochondria are the main source of ROS (Dostert et al 2008). Recent studies indicated that ROS could promote the activation of the NLRP3 inflammasome (Yin et al 2017). VDAC1 is a critical regulator of mitochondrial metabolic activity through the uptake of Ca 2?…”

Section: Nlrp3mentioning

confidence: 97%

Potential Roles of Mitochondria-Associated ER Membranes (MAMs) in Traumatic Brain Injury

Sun

Chen

et al. 2017

Cell Mol Neurobiol

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The endoplasmic reticulum (ER) and mitochondria have both been shown to be critical in cellular homeostasis. The functions of the ER and mitochondria are independent but interrelated. These two organelles could form physical interactions, known as MAMs, to regulate physiological functions between ER and mitochondria to maintain Ca, lipid, and metabolite exchange. Several proteins are located in MAMs, including RNA-dependent protein kinase (PKR)-like ER kinase, inositol 1,4,5-trisphosphate receptors, phosphofurin acidic cluster sorting protein-2 and sigma-1 receptor to ensure regulation. Recent studies indicated that MAMs participate in inflammation and apoptosis in various conditions. All of these functions are crucial in determining cell fate following traumatic brain injury (TBI). We hypothesized that MAMs may associate with TBI and could contribute to mitochondrial dysfunction, ER stress, autophagy dysregulation, dysregulation of Ca homeostasis, and oxidative stress. In this review, we summarize the latest understanding of MAM formation and their potential regulatory role in TBI pathophysiology.

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Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway

Cited by 102 publications

References 48 publications

Evidence and perspective for the role of the NLRP3 inflammasome signaling pathway in ischemic stroke and its therapeutic potential (Review)

Evidence and perspective for the role of the NLRP3 inflammasome signaling pathway in ischemic stroke and its therapeutic potential (Review)

Leptin promotes IL-18 secretion by activating the NLRP3 inflammasome in RAW 264.7 cells

Potential Roles of Mitochondria-Associated ER Membranes (MAMs) in Traumatic Brain Injury

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