NLRP3 inflammasome activation is associated with PM<sub>2.5</sub>‐induced cardiac functional and pathological injury in mice

Duan, Shuyin; Wang, Na; Huang, Li; Zhao, Ying; Shao, Hua; Jin, Yuefei; Zhang, Ruiqin; Li, Chunyang; Wu, Weidong; Wang, Jing; Feng, Feifei

doi:10.1002/tox.22825

Cited by 47 publications

(28 citation statements)

References 42 publications

(125 reference statements)

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“…The markers contain NLRP3, IL-1β, IL-18, Cleaved caspase-1 p10, while Cleaved IL-1β was upregulated in heart tissue of PM-induced mice. The results mean that PM2.5 exposure could induce structural and functional disorders, which might be linked to the NLRP3 inflammasome activation [49]. In an in vitro study, Shen et.al have proved that cooking oil fumes-derived PM2.5 could reduce HUVECs viability, induce the overproduction of ROS, which could affect the blood vessel formation through ROS-mediated NLRP3 inflammasome pathway [50].…”

Section: Pm25 and Pyroptosismentioning

confidence: 99%

PM2.5-related cell death patterns

Wang¹,

Zhong²,

Liao³

et al. 2021

Int. J. Med. Sci.

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With the increasingly serious problem of environmental pollution, the health problems caused by PM2.5 are gradually coming into our line of sight. Previous researches have indicated that air pollution is nearly related to various diseases, but few studies have focused on the exact function mediated by particulate matter less than 2.5 (PM2.5) in these diseases. PM2.5 is known to induce multiple ways of cell death, including autophagy, necrosis, apoptosis, pyroptosis and ferroptosis. Therefore, it is of much importance to understand the different ways of cell death caused by PM2.5 in the pathogenesis and treatment of PM2.5-related diseases. This present review is an insight of multiple ways of PM2.5-induced cell death in different diseases.

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Section: Pm25 and Pyroptosismentioning

confidence: 99%

PM2.5-related cell death patterns

Wang¹,

Zhong²,

Liao³

et al. 2021

Int. J. Med. Sci.

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“…The classical pyroptosis pathway is central to PM 2.5-induced injury. Previous studies have reported PM 2.5induced NLRP3 in ammasome activation and ocular injury in vivo and in vitro [15,23,24,25,26,27,28,29,30,31]. The NLRP3 in ammasome is a vital component of sterile-and infection-triggered in ammation as well as of the immune responses to various diseases [32].…”

Section: Discussionmentioning

confidence: 99%

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Xing

Niu

et al. 2021

Preprint

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Background Particulate matter (PM) is strongly linked to human health and has detrimental effects on the eye. Studies have, however, focused on the ocular surface, with limited research on the impact of PM2.5 on intraocular pressure (IOP).Methods To investigate the impact of PM2.5 on IOP and the associated mechanism, C57BL/6 mouse eyes were topically exposed to a PM2.5 suspension for 3 months, and human trabecular meshwork (HTM) cells were subjected to various PM2.5 concentrations in vitro.Results The results revealed that the IOP increased gradually after PM2.5 exposure, and an upregulation of NLRP3 inflammasome, caspase-1, IL-1β, and GSDMD protein levels was observed in outflow tissues. PM2.5 exposure decreased HTM cell viability and affected contraction. Further, elevated ROS levels were observed as well as an activation of the NLRP3 inflammasome and downstream inflammatory factors caspase-1 and IL-1β. ROS scavenger or caspase-1 inhibitor treatment improved these PM2.5-induced changes.Conclusion This study provides novel evidence of the PM2.5-mediated development of ocular hypertension, which occurs as a result of increased oxidative stress and the subsequent induction of pyroptosis in trabecular meshwork cells.

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“…PM 2.5 promotes HaCaT cells to synthesize and release TSLP, TNF-α, IL-1α, and IL-8, and upregulates the expression IL-1β and IL-18 in the heart tissue in mice 4 , 16 . Considering that several cytokines depend on the activation and maturation of inflammasomes, we supposed whether inflammasome is one of the products in skin cells upon PM 2.5 stimulation.…”

Section: Discussionmentioning

confidence: 99%

Fine Particulate Matter (PM_2.5) upregulates expression of Inflammasome NLRP1 via ROS/NF-κB signaling in HaCaT Cells

Liu

Yang

et al. 2020

Int. J. Med. Sci.

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Skin, as the major organ of a human body, is constantly exposed to PM2.5 stimulation, which may exert specific toxic influences on the physiology of skin. This study aims to investigate the effect of PM2.5 on the formation of inflammasomes in skin cells and to explore the potential mechanism linking PM2.5 and skin inflammation. Changes in mRNA and protein levels of inflammasome-related genes were detected by real-time PCR and western blot in human immortalized epidermal cells (HaCaT) treated with PM2.5 at multiple concentrations for 24 hours. The expression of NLRP1 was increased significantly both in mRNA and protein levels after PM2.5 exposure while the elevated secretory protein level of IL-1β in cell culture was detected by ELISA, which is one of the main downstream factors of NLRP1. In addition, the upregulation of NLRP1 and IL-1β could be reversed by NF-κB inhibitor indicating that PM2.5 may promote NLRP1 expression through activating NF-κB pathway. Furthermore, high ROS level was also found in cells treated with PM2.5 and inhibition of ROS could also reverse NK-κB production stimulated by PM2.5 that means ROS is involved in this skin inflammation process.

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NLRP3 inflammasome activation is associated with PM_2.5‐induced cardiac functional and pathological injury in mice

Cited by 47 publications

References 42 publications

PM2.5-related cell death patterns

PM2.5-related cell death patterns

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Fine Particulate Matter (PM_2.5) upregulates expression of Inflammasome NLRP1 via ROS/NF-κB signaling in HaCaT Cells

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NLRP3 inflammasome activation is associated with PM2.5‐induced cardiac functional and pathological injury in mice

Cited by 47 publications

References 42 publications

PM2.5-related cell death patterns

PM2.5-related cell death patterns

Airborne particulate matter (PM2.5) triggers ocular hypertension through pyroptosis

Fine Particulate Matter (PM2.5) upregulates expression of Inflammasome NLRP1 via ROS/NF-κB signaling in HaCaT Cells

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NLRP3 inflammasome activation is associated with PM_2.5‐induced cardiac functional and pathological injury in mice

Fine Particulate Matter (PM_2.5) upregulates expression of Inflammasome NLRP1 via ROS/NF-κB signaling in HaCaT Cells