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Title:
Endoplasmic reticulum stress may activate NLRP3 inflammasomes via TXNIP in preeclampsia | Cell and Tissue Research
Description:
Preeclampsia (PE) development is often associated with placental immune and inflammatory dysregulation, as well as endoplasmic reticulum (ER) stress. However, the mechanisms linking ER stress and inflammatory dysregulation to PE have not been elucidated. It has been reported that thioredoxin-interacting protein (TXNIP), which can bind with and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, is a key point in immune regulation. Recent experimental evidence suggests that activated NLRP3 inflammasomes can activate interleukin-1β (IL-1β) production in the placenta of patients with PE. The objective of the current study was to explore if TXNIP plays a critical signaling role linking ER stress with NLRP3 inflammasome activation in PE. We hypothesized that ER stress would induce TXNIP production, which would bind with NLRP3 inflammasomes to activate IL-1β production. These cells showed a higher protein level of NLRP3 and IL-1β, as well as a higher enzymatic activity of caspase-1, indicating enhanced inflammatory dysregulation and ER stress. Cells transfected with TXNIP siRNA showed reduced NLRP3 inflammasome activation. Cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, showed a similar result. Outgrowth of the explant with TXNIP lentivirus in H/R or tunicamycin (inducers of ER stress) was also measured to verify our hypothesis. These findings demonstrated that TXNIP could influence inflammatory dysregulation by mediating ER stress and NLRP3 inflammasome activation in PE. This novel mechanism may further explain the inflammation observed at the maternal-fetal interface, which leads to placental dysfunction in a patient with PE.
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article, google, scholar, preeclampsia, stress, nlrp, cas, endoplasmic, reticulum, txnip, inflammasome, cell, activate, published, inflammatory, research, inflammasomes, zhang, placenta, cells, chongqing, access, obstet, esm, png, high, resolution, image, tif, privacy, cookies, content, tissue, yang, jianxin, zhou, placental, protein, activation, human, gynecol, wang, china, information, publish, search, october, han, hongbo, hua,
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month download article/chapter grp78/perk/chop pathway bead-based multiplexed immunoassays tumor necrosis factor-alpha trophoblast htr-8/svneo cells endoplasmic reticulum stress related subjects targeting endoplasmic reticulum endoplasmic reticulum er inflammation endoplasmic reticulum mir-101 regulates apoptosis capsaicin-mediated tnox privacy choices/manage cookies full article pdf higher enzymatic activity critical inflammatory pathway thioredoxin-interacting protein human extravillous trophoblast activate il-1β production tissue research aims interleukin-1-beta polymorphisms national key research chngqing health center nlrp3 inflammasome activation chongqing health commission endoplasmic reticulum mediating er stress irremediable er stress human trophoblasts exposed european economic area ting-li han early onset preeclampsia acog practice bulletin araujo jp jr investigating trophoblast function zealand joint laboratory high resolution image placentally produced inflammatory higher protein level additional information publisher conditions privacy policy influence inflammatory dysregulation interleukin-1 receptor antagonist pre-eclampsia activate interleukin-1β activated nlrp3 inflammasomes hua zhang maternal-fetal interface accepting optional cookies article yang
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headline:Endoplasmic reticulum stress may activate NLRP3 inflammasomes via TXNIP in preeclampsia
description:Preeclampsia (PE) development is often associated with placental immune and inflammatory dysregulation, as well as endoplasmic reticulum (ER) stress. However, the mechanisms linking ER stress and inflammatory dysregulation to PE have not been elucidated. It has been reported that thioredoxin-interacting protein (TXNIP), which can bind with and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, is a key point in immune regulation. Recent experimental evidence suggests that activated NLRP3 inflammasomes can activate interleukin-1β (IL-1β) production in the placenta of patients with PE. The objective of the current study was to explore if TXNIP plays a critical signaling role linking ER stress with NLRP3 inflammasome activation in PE. We hypothesized that ER stress would induce TXNIP production, which would bind with NLRP3 inflammasomes to activate IL-1β production. These cells showed a higher protein level of NLRP3 and IL-1β, as well as a higher enzymatic activity of caspase-1, indicating enhanced inflammatory dysregulation and ER stress. Cells transfected with TXNIP siRNA showed reduced NLRP3 inflammasome activation. Cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, showed a similar result. Outgrowth of the explant with TXNIP lentivirus in H/R or tunicamycin (inducers of ER stress) was also measured to verify our hypothesis. These findings demonstrated that TXNIP could influence inflammatory dysregulation by mediating ER stress and NLRP3 inflammasome activation in PE. This novel mechanism may further explain the inflammation observed at the maternal-fetal interface, which leads to placental dysfunction in a patient with PE.
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Inflammation
Endoplasmic reticulum (ER) stress
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Human Genetics
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headline:Endoplasmic reticulum stress may activate NLRP3 inflammasomes via TXNIP in preeclampsia
description:Preeclampsia (PE) development is often associated with placental immune and inflammatory dysregulation, as well as endoplasmic reticulum (ER) stress. However, the mechanisms linking ER stress and inflammatory dysregulation to PE have not been elucidated. It has been reported that thioredoxin-interacting protein (TXNIP), which can bind with and activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome, is a key point in immune regulation. Recent experimental evidence suggests that activated NLRP3 inflammasomes can activate interleukin-1β (IL-1β) production in the placenta of patients with PE. The objective of the current study was to explore if TXNIP plays a critical signaling role linking ER stress with NLRP3 inflammasome activation in PE. We hypothesized that ER stress would induce TXNIP production, which would bind with NLRP3 inflammasomes to activate IL-1β production. These cells showed a higher protein level of NLRP3 and IL-1β, as well as a higher enzymatic activity of caspase-1, indicating enhanced inflammatory dysregulation and ER stress. Cells transfected with TXNIP siRNA showed reduced NLRP3 inflammasome activation. Cells treated with 4-phenylbutyric acid, an inhibitor of ER stress, showed a similar result. Outgrowth of the explant with TXNIP lentivirus in H/R or tunicamycin (inducers of ER stress) was also measured to verify our hypothesis. These findings demonstrated that TXNIP could influence inflammatory dysregulation by mediating ER stress and NLRP3 inflammasome activation in PE. This novel mechanism may further explain the inflammation observed at the maternal-fetal interface, which leads to placental dysfunction in a patient with PE.
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Inflammation
Endoplasmic reticulum (ER) stress
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Human Genetics
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name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, Peopleās Republic of China
name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, Peopleās Republic of China
name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, Peopleās Republic of China
name:College of Medicine, Biological Sciences and Psychology, University of Leicester, Leicester, UK
name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, Peopleās Republic of China
name:College of Medicine, Biological Sciences and Psychology, University of Leicester, Leicester, UK
name:Department of Obstetrics, Chngqing Health Center For Women And Children, Chongqing, Peopleās Republic of China
name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, Peopleās Republic of China
name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, Peopleās Republic of China
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Analytics and Tracking {š}
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Libraries {š}
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CDN Services {š¦}
- Crossref