| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Yael Alippe, Chun Wang, Biancamaria Ricci, Jianqiu Xiao, Chao Qu, Wei Zou, Deborah V Novack, Yousef Abu-Amer, Roberto Civitelli, Gabriel Mbalaviel. Bone matrix components activate the NLRP3 inflammasome and promote osteoclast differentiation. Scientific reports. vol 7. issue 1. 2019-02-04. PMID:28747793. |
the nlrp3 inflammasome senses a variety of signals referred to as danger associated molecular patterns (damps), including those triggered by crystalline particulates or degradation products of extracellular matrix. |
2019-02-04 |
2023-08-13 |
mouse |
| Yael Alippe, Chun Wang, Biancamaria Ricci, Jianqiu Xiao, Chao Qu, Wei Zou, Deborah V Novack, Yousef Abu-Amer, Roberto Civitelli, Gabriel Mbalaviel. Bone matrix components activate the NLRP3 inflammasome and promote osteoclast differentiation. Scientific reports. vol 7. issue 1. 2019-02-04. PMID:28747793. |
since some damps confer tissue-specific activation of the inflammasomes, we tested the hypothesis that bone matrix components function as damps for the nlrp3 inflammasome and regulate osteoclast differentiation. |
2019-02-04 |
2023-08-13 |
mouse |
| Yael Alippe, Chun Wang, Biancamaria Ricci, Jianqiu Xiao, Chao Qu, Wei Zou, Deborah V Novack, Yousef Abu-Amer, Roberto Civitelli, Gabriel Mbalaviel. Bone matrix components activate the NLRP3 inflammasome and promote osteoclast differentiation. Scientific reports. vol 7. issue 1. 2019-02-04. PMID:28747793. |
thus, signals originating from bone matrix activate the nlrp3 inflammasome in the osteoclast lineage, and may represent a bone-restricted positive feedback mechanism that amplifies bone resorption in pathologic conditions of accelerated bone turnover. |
2019-02-04 |
2023-08-13 |
mouse |
| Dietmar Spengler, Supandi Winoto-Morbach, Sarah Kupsch, Christina Vock, Katharina Blöchle, Susanna Frank, Nele Rintz, Marie Diekötter, Harshavardhan Janga, Markus Weckmann, Sabine Fuchs, Andra B Schromm, Heinz Fehrenbach, Stefan Schütze, Martin F Kraus. Novel therapeutic roles for surfactant-inositols and -phosphatidylglycerols in a neonatal piglet ARDS model: a translational study. American journal of physiology. Lung cellular and molecular physiology. vol 314. issue 1. 2019-01-10. PMID:28860142. |
the inositol derivatives (mainly s+ip3) exerted their actions by suppressing acid sphingomyelinase activity and dependent ceramide production, linked with the suppression of the inflammasome nucleotide-binding domain, leucine-rich repeat-containing protein-3 (nlrp3)-apoptosis-associated speck-like protein containing a caspase recruitment domain (asc)-caspase-1 complex, and the profibrotic response represented by the cytokines transforming growth factor-β1 and ifn-γ, matrix metalloproteinase (mmp)-1/8, and elastin. |
2019-01-10 |
2023-08-13 |
Not clear |
| Xiaoguang Zhu, Jun Shi, Huicong L. Liquiritigenin attenuates high glucose-induced mesangial matrix accumulation, oxidative stress, and inflammation by suppression of the NF-κB and NLRP3 inflammasome pathways. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. vol 106. 2018-12-18. PMID:30119269. |
liquiritigenin attenuates high glucose-induced mesangial matrix accumulation, oxidative stress, and inflammation by suppression of the nf-κb and nlrp3 inflammasome pathways. |
2018-12-18 |
2023-08-13 |
Not clear |
| Chongfeng Bai, Tao Li, Qing Sun, Qun Xin, Tongyi Xu, Jinjian Yu, Yun Wang, Li We. Protective effect of baicalin against severe burn‑induced remote acute lung injury in rats. Molecular medicine reports. vol 17. issue 2. 2018-07-17. PMID:29207058. |
as a result, baicalin significantly suppressed nucleotide‑binding oligomerization, nacht, lrr and pyd domains‑containing protein 3 (nlrp3), caspase‑1, nuclear factor‑κb and matrix metalloproteinase‑9 protein expression in the rat model of ali. |
2018-07-17 |
2023-08-13 |
rat |
| Ana S Falcão, Luís A R Carvalho, Gonçalo Lidónio, Ana R Vaz, Susana D Lucas, Rui Moreira, Dora Brite. Dipeptidyl Vinyl Sulfone as a Novel Chemical Tool to Inhibit HMGB1/NLRP3-Inflammasome and Inflamma-miRs in Aβ-Mediated Microglial Inflammation. ACS chemical neuroscience. vol 8. issue 1. 2017-10-30. PMID:27797173. |
vs also suppressed aβ-induced expression of inflammatory mediators in microglia, such as matrix metalloproteinase (mmp)-2 and mmp-9, as well as high-mobility group box protein-1 (hmgb1), nod-like receptor protein 3 (nlrp3)-inflammasome, and interleukin (il)-1β. |
2017-10-30 |
2023-08-13 |
mouse |
| Wei Gong, Song Mao, Jing Yu, Jiayu Song, Zhanjun Jia, Songming Huang, Aihua Zhan. NLRP3 deletion protects against renal fibrosis and attenuates mitochondrial abnormality in mouse with 5/6 nephrectomy. American journal of physiology. Renal physiology. vol 310. issue 10. 2017-06-27. PMID:26887832. |
strikingly, tubulointerstitial fibrosis was remarkably attenuated in nlrp3(-/-) mice as evidenced by the blockade of extracellular matrix deposition. |
2017-06-27 |
2023-08-13 |
mouse |
| Wentao Liu, Toru Yamashita, Tomoko Kurata, Syoichiro Kono, Nozomi Hishikawa, Kentaro Deguchi, Yun Zhai, Koji Ab. Protective effect of telmisartan on neurovascular unit and inflammasome in stroke-resistant spontaneously hypertensive rats. Neurological research. vol 37. issue 6. 2016-02-29. PMID:25591419. |
we inspected the effect of telmisartan on the neurovascular unit (nvu) and related inflammatory responses in spontaneously hypertensive rat stroke resistant (shr-sr) by observing the components of nvu such as n-acetyl glucosamine oligomer (nago), collagen iv, astrocytes, and matrix metalloproteinase-9 (mmp-9), as well as inflammasome nod-like receptors family protein 3 (nlrp3). |
2016-02-29 |
2023-08-13 |
rat |
| Kathy Triantafilou, Timothy R Hughes, Martha Triantafilou, B Paul Morga. The complement membrane attack complex triggers intracellular Ca2+ fluxes leading to NLRP3 inflammasome activation. Journal of cell science. vol 126. issue Pt 13. 2014-01-16. PMID:23613465. |
this increase in intracellular ca(2+) concentration leads to ca(2+) accumulation in the mitochondrial matrix via the 'mitochondrial calcium uniporter' (mcu), and loss of mitochondrial transmembrane potential, triggering nlrp3 inflammasome activation and il-1β release. |
2014-01-16 |
2023-08-12 |
Not clear |
| Wenjie Wang, Xiangyu Wang, Justin Chun, Akosua Vilaysane, Sharon Clark, Gabrielle French, Nathan A Bracey, Kiril Trpkov, Shirin Bonni, Henry J Duff, Paul L Beck, Daniel A Muruv. Inflammasome-independent NLRP3 augments TGF-β signaling in kidney epithelium. Journal of immunology (Baltimore, Md. : 1950). vol 190. issue 3. 2013-03-26. PMID:23264657. |
in human and mouse primary renal tecs, nlrp3 expression was increased in response to tgf-β1 stimulation and associated with epithelial-mesenchymal transition (emt) and the expression of α-smooth muscle actin (αsma) and matrix metalloproteinase (mmp) 9. |
2013-03-26 |
2023-08-12 |
mouse |
| Robert Zeiser, Olaf Penack, Ernst Holler, Marco Idzk. Danger signals activating innate immunity in graft-versus-host disease. Journal of molecular medicine (Berlin, Germany). vol 89. issue 9. 2011-12-08. PMID:21573893. |
besides atp, uric acid or soluble extracellular matrix components are functional danger signals that activate the nlrp3 inflammasome when released from dying cells or from extracellular matrix. |
2011-12-08 |
2023-08-12 |
Not clear |
| Andrea Babelova, Kristin Moreth, Wasiliki Tsalastra-Greul, Jinyang Zeng-Brouwers, Oliver Eickelberg, Marian F Young, Peter Bruckner, Josef Pfeilschifter, Roland M Schaefer, Hermann-Josef Gröne, Liliana Schaefe. Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. The Journal of biological chemistry. vol 284. issue 36. 2009-10-05. PMID:19605353. |
our results provide evidence for direct activation of the nlrp3 inflammasome by biglycan and describe a fundamental paradigm of how tissue stress or injury is monitored by innate immune receptors detecting the release of the extracellular matrix components and turning such a signal into a robust inflammatory response. |
2009-10-05 |
2023-08-12 |
mouse |