ArticleFrontiers in bioscience (Landmark edition)2016
Instant membrane resealing in nlrp3 inflammmasome activation of endothelial cells.
Article in Frontiers in bioscience (Landmark edition), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Role of NLRP3 Inflammasome Inhibitors in Endothelial Dysfunction and Vascular Repair.Antioxidants (Basel, Switzerland) · 2026Review
- Impairment of Ceramide-Mediated Endothelial Instant Membrane Resealing During Diabetes Mellitus.Frontiers in physiology · 2022Article
- The roles of autophagy and thyroid hormone in the pathogenesis and treatment of NAFLD.Hepatoma research · 2021Article
- Thyroid Hormones Interaction With Immune Response, Inflammation and Non-thyroidal Illness Syndrome.Frontiers in cell and developmental biology · 2020Review
- Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways.Frontiers in cell and developmental biology · 2020Review
- Aspirin alleviates endothelial gap junction dysfunction through inhibition of NLRP3 inflammasome activation in LPS-induced vascular injury.Acta pharmaceutica Sinica. B · 2019Article
- Crosstalk Between Acid Sphingomyelinase and Inflammasome Signaling and Their Emerging Roles in Tissue Injury and Fibrosis.Frontiers in cell and developmental biology · 2019Review
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The present study explored the molecular mechanisms by which instant cell membrane resealing (CMR) controls the activation of NOD-like receptor pyrin domain containing 3 (Nlrp3) inflammasomes. Using wavelength-switching fluorescent microscopy with PI and fura-2 as indicators, we monitored instant CMR simultaneously with (Ca(2+))i in mouse microvascular endothelial cell (MVECs). LCWE or saponin wad found to produce membrane injury, which was resealed in a Ca(2+)-dependent manner, but abolished by FasL, a membrane raft (MR) clustering stimulator. Even in the presence of Ca(2+), FasL prolonged the CMR time as shown by an earlier onset of PI influx (48±12 sec vs. 17±3 min. of control). These effects of FasL were substantially blocked by an MR disruptor, methyl-beta-cyclodextrin (MCD). The failure of CMR upon FasL activated Nlrp3 inflammasomes, which was blocked by MCD, a membrane resealing compound, VA64 or siRNA of an MR-facilitating enzyme, acid sphingomyelinase. This inflammasome activation was due to increased lysosomal permeability and cathepsin B release. It is concluded that an MR-associated CMR protects ECs from Nlrp3 inflammasome activation induced by membrane injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.