scholarly journals The Overexpression of Sirtuin1 (SIRT1) Alleviated Lipopolysaccharide (LPS)-Induced Acute Kidney Injury (AKI) via Inhibiting the Activation of Nucleotide-Binding Oligomerization Domain-Like Receptors (NLR) Family Pyrin Domain Containing 3 (NLRP3) Inflammasome

2019 ◽  
Vol 25 ◽  
pp. 2718-2726 ◽  
Author(s):  
Qiufang Gao ◽  
Hengting Zhu
Keyword(s):  
Acute Kidney Injury ◽  
Nlrp3 Inflammasome ◽  
Kidney Injury ◽  
Nucleotide Binding ◽  
Pyrin Domain ◽  
Oligomerization Domain

scholarly journals The Complex Interplay between Autophagy and NLRP3 Inflammasome in Renal Diseases

2021 ◽  
Vol 22 (23) ◽  
pp. 12766
Author(s):  
Yong Ding ◽  
Xiaodi Fu ◽  
Qimeng Wang ◽  
Huiyang Liu ◽  
Honggang Wang ◽  
...  
Keyword(s):  
Nlrp3 Inflammasome ◽  
Basic Research ◽  
Nucleotide Binding ◽  
Eukaryotic Cell ◽  
Renal Diseases ◽  
Complex Interplay ◽  
Pyrin Domain ◽  
The Family ◽  
Receptor Family ◽  
Oligomerization Domain

Autophagy is a highly conserved process of the eukaryotic cell cycle. It plays an important role in the survival and maintenance of cells by degrading organelles, proteins, and macromolecules in the cytoplasm and the circulation of degraded products. The dysfunction of autophagy can lead to the pathology of many human diseases. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome belongs to the family of nucleotide-binding and oligomerization domain-like receptors (NLRs) and can induce caspase-1 activation, thus leading to the maturation and secretion of interleukin-1beta (IL-1β) and IL-18. It has been reported that the interplay between autophagy and NLRP3 inflammasome is involved in many diseases, including renal diseases. In this review, the interplay between autophagy and the NLRP3 inflammasome and the mechanisms in renal diseases are explored to provide ideas for relevant basic research in the future.

scholarly journals Upregulation of Nucleotide-Binding Oligomerization Domain-, LRR- and Pyrin Domain-Containing Protein 3 in Motoneurons Following Peripheral Nerve Injury in Mice

2020 ◽  
Vol 11 ◽  
Author(s):  
Bernát Nógrádi ◽  
Ádám Nyúl-Tóth ◽  
Mihály Kozma ◽  
Kinga Molnár ◽  
Roland Patai ◽  
...  
Keyword(s):  
Nerve Injury ◽  
Motor Neurons ◽  
Nucleotide Binding ◽  
Inflammasome Activation ◽  
Neuroprotective Effects ◽  
Pyrin Domain ◽  
Basal Expression ◽  
Wide Range ◽  
Treatment Paradigm ◽  
Oligomerization Domain

Neuronal injuries are accompanied by release and accumulation of damage-associated molecules, which in turn may contribute to activation of the immune system. Since a wide range of danger signals (including endogenous ones) are detected by the nucleotide-binding oligomerization domain-, LRR- and pyrin domain-containing protein 3 (NLRP3) pattern recognition receptor, we hypothesized that NLRP3 may become activated in response to motor neuron injury. Here we show that peripheral injury of the oculomotor and the hypoglossal nerves results in upregulation of NLRP3 in corresponding motor nuclei in the brainstem of mice. Although basal expression of NLRP3 was observed in microglia, astroglia and neurons as well, its upregulation and co-localization with apoptosis-associated speck-like protein containing a caspase activation and recruitment domain, suggesting inflammasome activation, was only detected in neurons. Consequently, increased production of active pro-inflammatory cytokines interleukin-1β and interleukin-18 were detected after hypoglossal nerve axotomy. Injury-sensitive hypoglossal neurons responded with a more pronounced NLRP3 upregulation than injury-resistant motor neurons of the oculomotor nucleus. We further demonstrated that the mitochondrial protector diazoxide was able to reduce NLRP3 upregulation in a post-operative treatment paradigm. Our results indicate that NLRP3 is activated in motoneurons following acute nerve injury. Blockade of NLRP3 activation might contribute to the previously observed anti-inflammatory and neuroprotective effects of diazoxide.

scholarly journals Intravenous Arginine Administration Downregulates NLRP3 Inflammasome Activity and Attenuates Acute Kidney Injury in Mice with Polymicrobial Sepsis

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Sharon Angela Tanuseputero ◽  
Ming-Tsan Lin ◽  
Sung-Ling Yeh ◽  
Chiu-Li Yeh
Keyword(s):  
Acute Kidney Injury ◽  
Protein Expression ◽  
Kidney Function ◽  
Nlrp3 Inflammasome ◽  
Cecal Ligation ◽  
Kidney Injury ◽  
Major Complication ◽  
Receptor Protein ◽  
No Production ◽  
Inflammasome Activity

Acute kidney injury (AKI) is a major complication of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasomes are multiprotein complexes that mediate septic AKI. L-arginine (Arg) is a conditionally essential amino acid in catabolic conditions and a substrate for nitric oxide (NO) production; however, its use in sepsis is controversial. This study investigated the effect of intravenous Arg supplementation on modulating NLRP3 inflammasome activity in relation to septic AKI. Mice were divided into normal control (NC), sham, sepsis saline (SS), and sepsis Arg (SA) groups. In order to investigate the role of NO, L-N6-(1-iminoethyl)-lysine hydrochloride (L-NIL), an inducible NO synthase inhibitor, was administered to the sepsis groups. Sepsis was induced using cecal ligation and puncture (CLP). The SS and SA groups received saline or Arg via tail vein 1 h after CLP. Mice were sacrificed at 6, 12, and 24 h after sepsis. The results showed that compared to the NC group, septic mice had higher plasma kidney function parameters and lower Arg levels. Also, renal NLRP3 inflammasome protein expression and tubular injury score increased. After Arg treatment, plasma Arg and NO levels increased, kidney function improved, and expressions of renal NLRP3 inflammasome-related proteins were downregulated. Changes in plasma NO and renal NLRP3 inflammasome-related protein expression were abrogated when L-NIL was given to the Arg sepsis groups. Arg plus L-NIL administration also attenuated kidney injury after CLP. The findings suggest that intravenous Arg supplementation immediately after sepsis restores plasma Arg levels and is beneficial for attenuating septic AKI, partly via NO-mediated NLRP3 inflammasome inhibition.

scholarly journals Role of the nucleotide-binding domain-like receptor protein 3 inflammasome in acute kidney injury

FEBS Journal ◽  
2015 ◽  
Vol 282 (19) ◽  
pp. 3799-3807 ◽  
Author(s):  
Yanhui Cao ◽  
Dongsheng Fei ◽  
Mingwei Chen ◽  
Miao Sun ◽  
Jun Xu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Nucleotide Binding ◽  
Binding Domain ◽  
Receptor Protein ◽  
Nucleotide Binding Domain

scholarly journals NLRP3 inflammasome mediates contrast media-induced acute kidney injury by regulating cell apoptosis

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jianxiao Shen ◽  
Ling Wang ◽  
Na Jiang ◽  
Shan Mou ◽  
Minfang Zhang ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Contrast Media ◽  
Nlrp3 Inflammasome ◽  
Cell Apoptosis ◽  
Kidney Injury
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