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  1. Analyzed Page
  2. Matching Content Categories
  3. CMS
  4. Monthly Traffic Estimate
  5. How Does Link.springer.com Make Money
  6. Keywords
  7. Topics
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We are analyzing https://link.springer.com/article/10.1007/s00441-019-03104-9.

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.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {šŸ“š}

  • Careers
  • Education
  • Health & Fitness

Content Management System {šŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {šŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {šŸ’ø}

We're unsure how the site profits.

Websites don't always need to be profitable; some serve as platforms for education or personal expression. Websites can serve multiple purposes. And this might be one of them. Link.springer.com might be earning cash quietly, but we haven't detected the monetization method.

Keywords {šŸ”}

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,

Topics {āœ’ļø}

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

Schema {šŸ—ŗļø}

WebPage:
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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.
         datePublished:2019-10-22T00:00:00Z
         dateModified:2019-12-07T00:00:00Z
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            Inflammation
            Endoplasmic reticulum (ER) stress
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            TXNIP
            Human Genetics
            Proteomics
            Molecular Medicine
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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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      dateModified:2019-12-07T00:00:00Z
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      pageEnd:599
      sameAs:https://doi.org/10.1007/s00441-019-03104-9
      keywords:
         Preeclampsia (PE)
         Inflammation
         Endoplasmic reticulum (ER) stress
         NLRP3
         TXNIP
         Human Genetics
         Proteomics
         Molecular Medicine
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      name:Jianxin Li
      affiliation:
            name:Chngqing Health Center For Women And Children
            address:
               name:Department of Obstetrics, Chngqing Health Center For Women And Children, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:The First Affiliated Hospital of Chongqing Medical University
            address:
               name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Ting-Li Han
      affiliation:
            name:The First Affiliated Hospital of Chongqing Medical University
            address:
               name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Xianbo Zhou
      affiliation:
            name:The First Affiliated Hospital of Chongqing Medical University
            address:
               name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Hongbo Qi
      affiliation:
            name:The First Affiliated Hospital of Chongqing Medical University
            address:
               name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:University of Leicester
            address:
               name:College of Medicine, Biological Sciences and Psychology, University of Leicester, Leicester, UK
               type:PostalAddress
            type:Organization
      name:Philip N. Baker
      affiliation:
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:University of Leicester
            address:
               name:College of Medicine, Biological Sciences and Psychology, University of Leicester, Leicester, UK
               type:PostalAddress
            type:Organization
      name:Wei Zhou
      affiliation:
            name:Chngqing Health Center For Women And Children
            address:
               name:Department of Obstetrics, Chngqing Health Center For Women And Children, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Hua Zhang
      affiliation:
            name:The First Affiliated Hospital of Chongqing Medical University
            address:
               name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
            name:Chongqing Medical University
            address:
               name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Obstetrics, Chngqing Health Center For Women And Children, Chongqing, People’s Republic of China
      name:Department of Obstetrics, Chngqing Health Center For Women And Children, Chongqing, People’s Republic of China
      name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
      name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
      name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
      name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
      name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
      name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
      name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
      name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s 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, People’s 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, People’s Republic of China
      name:Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China
      name:Canada - China -New Zealand Joint Laboratory of Maternal and Fetal Medicine, Chongqing Medical University, Chongqing, People’s Republic of China
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