ArticlePharmaceuticals (Basel, Switzerland)2022
Tunicamycin Protects against LPS-Induced Lung Injury.
Article in Pharmaceuticals (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- IL-1βCell death discovery · 2025Article
- AZD6738 Attenuates LPS-Induced Corneal Inflammation and Fibrosis by Modulating Macrophage Function and Polarization.Inflammation · 2025Article
- Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025Review
- Unfolded protein response modulates the effects of GHRH antagonists in experimental models ofTissue barriers · 2025Article
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- Unfolded protein response suppression potentiates LPS-induced barrier dysfunction and inflammation in bovine pulmonary artery endothelial cells.Tissue barriers · 2024Article
- Article
- Unrealized targets in the discovery of antibiotics for Gram-negative bacterial infections.Nature reviews. Drug discovery · 2023Review
- Ceapin-A7 potentiates lipopolysaccharide-induced endothelial injury.Journal of biochemical and molecular toxicology · 2023Article
- Pneumonic Injury and Repair: A Synopsis.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Growth hormone-releasing hormone antagonists protect against hydrochloric acid-induced endothelial injury in vitro.Environmental toxicology and pharmacology · 2023Article
- Growth Hormone-Releasing Hormone Antagonist JV-1-36 Suppresses Reactive Oxygen Species Generation in A549 Lung Cancer Cells.Endocrines · 2022Article
- P53 in endothelial function and unfolded protein response regulation.Cell biology international · 2022Article
- Activating transcription factor 6 protects against endothelial barrier dysfunction.Cellular signalling · 2022Article
- Unfolded protein response in endothelial injury.Cell cycle (Georgetown, Tex.) · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The pulmonary endothelium is a dynamic semipermeable barrier that orchestrates tissue-fluid homeostasis; regulating physiological and immunological responses. Endothelial abnormalities are caused by inflammatory stimuli interacting with intracellular messengers to remodel cytoskeletal junctions and adhesion proteins. Those phenomena are associated with sepsis, acute lung injury, and acute respiratory distress syndrome. The molecular processes beyond those responses are the main interest of our group. Unfolded protein response (UPR) is a highly conserved molecular pathway resolving protein-folding defects to counteract cellular threats. An emerging body of evidence suggests that UPR is a promising target against lung and cardiovascular disease. In the present study, we reveal that Tunicamycin (TM) (UPR inducer) protects against lipopolysaccharide (LPS)-induced injury. The barrier function of the inflamed endothelium was evaluated in vitro (transendothelial and paracellular permeability); as well as in mice exposed to TM after LPS. Our study demonstrates that TM supports vascular barrier function by modulating actomyosin remodeling. Moreover, it reduces the internalization of vascular endothelial cadherin (VE-cadherin), enhancing endothelial integrity. We suggest that UPR activation may deliver novel therapeutic opportunities in diseases related to endothelial dysregulation.
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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.