ArticlePloS one2013
Lipopolysaccharide induces endoplasmic store Ca2+-dependent inflammatory responses in lung microvessels.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- The emerging role of neutrophil extracellular traps in ulcerative colitis.Frontiers in immunology · 2024Review
- NMDARs antagonist MK801 suppresses LPS-induced apoptosis and mitochondrial dysfunction by regulating subunits of NMDARs via the CaM/CaMKII/ERK pathway.Cell death discovery · 2023Article
- The role of G protein-coupled receptor in neutrophil dysfunction during sepsis-induced acute respiratory distress syndrome.Frontiers in immunology · 2023Review
- Toll-like receptor 4 activation enhances Orai1-mediated calcium signal promoting cytokine production in spinal astrocytes.Cell calcium · 2022Article
- Human umbilical cord mesenchymal stem cell-derived mitochondria (PN-101) attenuate LPS-induced inflammatory responses by inhibiting NFκB signaling pathway.BMB reports · 2022Article
- Gasdermin D pores are dynamically regulated by local phosphoinositide circuitry.Nature communications · 2022Article
- Mechanosensitive cation channel Piezo1 contributes to ventilator-induced lung injury by activating RhoA/ROCK1 in rats.Respiratory research · 2021Article
- The Effects of Insulin-Like Growth Factor I and BTP-2 on Acute Lung Injury.International journal of molecular sciences · 2021Article
- TAS2R16 Activation Suppresses LPS-Induced Cytokine Expression in Human Gingival Fibroblasts.Frontiers in immunology · 2021Article
- Cellular Mechanisms of NETosis.Annual review of cell and developmental biology · 2020Review
- IGF-1 Deficiency Rescue and Intracellular Calcium Blockade Improves Survival and Corresponding Mechanisms in a Mouse Model of Acute Kidney Injury.International journal of molecular sciences · 2020Article
- Mibefradil and Flunarizine, Two T-Type Calcium Channel Inhibitors, Protect Mice against Lipopolysaccharide-Induced Acute Lung Injury.Mediators of inflammation · 2020Article
- Anti-Inflammatory Properties ofMolecules (Basel, Switzerland) · 2019Article
- Endothelial Cdc42 deficiency impairs endothelial regeneration and vascular repair after inflammatory vascular injury.Respiratory research · 2018Article
- Thrombin Induces Inositol Trisphosphate-Mediated Spatially Extensive Responses in Lung Microvessels.The American journal of pathology · 2017Article
- Changes in endothelial connexin 43 expression inversely correlate with microvessel permeability and VE-cadherin expression in endotoxin-challenged lungs.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Myeloperoxidase evokes substantial vasomotor responses in isolated skeletal muscle arterioles of the rat.Acta physiologica (Oxford, England) · 2015Article
- Cooperative signaling via transcription factors NF-κB and AP1/c-Fos mediates endothelial cell STIM1 expression and hyperpermeability in response to endotoxin.The Journal of biological chemistry · 2014Article
- Quantifying single microvessel permeability in isolated blood-perfused rat lung preparation.Journal of visualized experiments : JoVE · 2014Article
- Aging mesenchymal stem cells fail to protect because of impaired migration and antiinflammatory response.American journal of respiratory and critical care medicine · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The pulmonary microvasculature plays a critical role in endotoxin-induced acute lung injury. However, the relevant signaling remain unclear. Specifically the role of endothelial Ca(2+) in the induction of endotoxin-mediated responses in lung microvessels remains undefined. Toward elucidating this, we used the isolated blood-perfused rat lung preparation. We loaded microvessels with the Ca(2+) indicator, Fura 2 AM and then determined Ca(2+) responses to infusions of lipopolysaccharide (LPS) into the microvessels. LPS induced a more than two-fold increase in the amplitude of cytosolic Ca(2+) oscillations. Inhibiting inositol 1,4,5 trisphosphate receptors on endoplasmic reticulum (ER) Ca(2+) stores with Xestospongin C (XeC), blocked the LPS-induced increase in the Ca(2+) oscillation amplitude. However, XeC did not affect entry of external Ca(2+) via plasma membrane Ca(2+) channels in lung microvascular endothelial cells. This suggested that LPS augmented the oscillations via release of Ca(2+) from ER stores. In addition, XeC also blocked LPS-mediated activation and nuclear translocation of nuclear factor-kappa B in lung microvessels. Further, inhibiting ER Ca(2+) release blunted increases in intercellular adhesion molecule-1 expression and retention of naïve leukocytes in LPS-treated microvessels. Taken together, the data suggest that LPS-mediated Ca(2+) release from ER stores underlies nuclear factor-kappa B activation and downstream inflammatory signaling in lung microvessels. Thus, we show for the first time a role for inositol 1,4,5 trisphosphate-mediated ER Ca(2+) release in the induction of LPS responses in pulmonary microvascular endothelium. Mechanisms that blunt this signaling may mitigate endotoxin-induced morbidity.
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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.