NADPH oxidases regulate endothelial inflammatory injury induced by PM 2.5 via AKT/eNOS/NO axis

2021 ◽  
Author(s):  
Lingyue Zou ◽  
Lilin Xiong ◽  
Tianshu Wu ◽  
Tingting Wei ◽  
Na Liu ◽  
...  
Keyword(s):  
Nadph Oxidases ◽  
Inflammatory Injury ◽  
Pm 2.5

NADPH Containing Protein Component from Fruits and Plant: Stimulation of NADPH Oxidases of Immune Cells

2020 ◽  
Vol 56 (7) ◽  
pp. 800-800
Author(s):  
R. M. Simonyan ◽  
K. V. Simonyan ◽  
S. M. Feschyan ◽  
V. A. Chavushyan ◽  
G. M. Simonyan ◽  
...  
Keyword(s):  
Immune Cells ◽  
Protein Component ◽  
Nadph Oxidases ◽  
Stimulation Of

Metalloproteinases, Sialidases and NADPH Oxidases as Key Enzymes involved in Atherosclerosis Development

2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Anastasia V Poznyak ◽  
Dmitry A Kashirskikh ◽  
Victoria A Khotina ◽  
Andrey V Grechko ◽  
Alexander N Orekhov
Keyword(s):  
Nadph Oxidases ◽  
Key Enzymes ◽  
Atherosclerosis Development

scholarly journals Jagged1-mediated myeloid Notch1 signaling activates HSF1/Snail and controls NLRP3 inflammasome activation in liver inflammatory injury

2019 ◽  
Vol 17 (12) ◽  
pp. 1245-1256 ◽  
Author(s):  
Yuting Jin ◽  
Changyong Li ◽  
Dongwei Xu ◽  
Jianjun Zhu ◽  
Song Wei ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Immune Cell ◽  
Ischemia Reperfusion ◽  
Inflammasome Activation ◽  
Inflammatory Injury ◽  
Notch1 Signaling ◽  
Caspase 1 ◽  
Hepatocellular Damage ◽  
Hepatocellular Apoptosis

AbstractNotch signaling plays important roles in the regulation of immune cell functioning during the inflammatory response. Activation of the innate immune signaling receptor NLRP3 promotes inflammation in injured tissue. However, it remains unknown whether Jagged1 (JAG1)-mediated myeloid Notch1 signaling regulates NLRP3 function in acute liver injury. Here, we report that myeloid Notch1 signaling regulates the NLRP3-driven inflammatory response in ischemia/reperfusion (IR)-induced liver injury. In a mouse model of liver IR injury, Notch1-proficient (Notch1FL/FL) mice receiving recombinant JAG1 showed a reduction in IR-induced liver injury and increased Notch intracellular domain (NICD) and heat shock transcription factor 1 (HSF1) expression, whereas myeloid-specific Notch1 knockout (Notch1M-KO) aggravated hepatocellular damage even with concomitant JAG1 treatment. Compared to JAG1-treated Notch1FL/FL controls, Notch1M-KO mice showed diminished HSF1 and Snail activity but augmented NLRP3/caspase-1 activity in ischemic liver. The disruption of HSF1 reduced Snail activation and enhanced NLRP3 activation, while the adoptive transfer of HSF1-expressing macrophages to Notch1M-KO mice augmented Snail activation and mitigated IR-triggered liver inflammation. Moreover, the knockdown of Snail in JAG1-treated Notch1FL/FL livers worsened hepatocellular functioning, reduced TRX1 expression and increased TXNIP/NLRP3 expression. Ablation of myeloid Notch1 or Snail increased ASK1 activation and hepatocellular apoptosis, whereas the activation of Snail increased TRX1 expression and reduced TXNIP, NLRP3/caspase-1, and ROS production. Our findings demonstrated that JAG1-mediated myeloid Notch1 signaling promotes HSF1 and Snail activation, which in turn inhibits NLRP3 function and hepatocellular apoptosis leading to the alleviation of IR-induced liver injury. Hence, the Notch1/HSF1/Snail signaling axis represents a novel regulator of and a potential therapeutic target for liver inflammatory injury.

Exercise Performed Concomitantly with Particulate Matter Exposure Inhibits Lung Injury

2017 ◽  
Vol 39 (02) ◽  
pp. 133-140 ◽  
Author(s):  
Adriano Silva-Renno ◽  
Guilherme Baldivia ◽  
Manoel Oliveira-Junior ◽  
Maysa Brandao-Rangel ◽  
Elias El-Mafarjeh ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Systemic Inflammation ◽  
Air Pollutants ◽  
Lung Parenchyma ◽  
Treadmill Training ◽  
Tnf Alpha ◽  
Systemic Response ◽  
Pm 2.5 ◽  
Pm 10 ◽  
Particulate Matter Exposure

AbstractAir pollution is a growing problem worldwide, inducing and exacerbating several diseases. Among the several components of air pollutants, particulate matter (PM), especially thick (10–2.5 µm; PM 10) and thin (≤2.5 µm; PM 2.5), are breathable particles that easily can be deposited within the lungs, resulting in pulmonary and systemic inflammation. Although physical activity is strongly recommended, its effects when practiced in polluted environments are questionable. Therefore, the present study evaluated the pulmonary and systemic response of concomitant treadmill training with PM 2.5 and PM 10 exposure. Treadmill training inhibited PM 2.5- and PM 10-induced accumulation of total leukocytes (p<0.001), neutrophils (p<0.001), macrophages (p<0.001) and lymphocytes (p<0.001) in bronchoalveolar lavage (BAL), as well as the BAL levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.05). Similar effects were observed on accumulation of polymorphonuclear (p<0.01) and mononuclear (p<0.01) cells in the lung parenchyma and in the peribronchial space. Treadmill training also inhibited PM 2.5- and PM 10-induced systemic inflammation, as observed in the number of total leukocytes (p<0.001) and in the plasma levels of IL-1beta (p<0.001), CXCL1/KC (p<0.001) and TNF-alpha (p<0.001), whereas it increased IL-10 levels (p<0.001). Treadmill training inhibits lung and systemic inflammation induced by particulate matter.

Sign in / Sign up

Export Citation Format

Share Document