ArticleCellular signalling2022
Activating transcription factor 6 protects against endothelial barrier dysfunction.
Article in Cellular signalling, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Somatostatin analogs in endothelial dysfunction.American journal of physiology. Endocrinology and metabolism · 2025Article
- ATF6 Alleviates Endothelial Inflammation Following Extended Hepatectomy Through Inhibition of TRIM10/NF-κB Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Growth hormone - releasing hormone in the immune system.Reviews in endocrine & metabolic disorders · 2025Review
- Orchestration of SARS-CoV-2 Nsp4 and host cell ESCRT proteins induces morphological changes of the endoplasmic reticulum.Molecular biology of the cell · 2025Article
- Article
- Unfolded protein responses: Dynamic machinery in wound healing.Pharmacology & therapeutics · 2025Review
- ATF6 inhibition suppresses the protective effects of pasireotide in human and bovine endothelial cells.Vascular biology (Bristol, England) · 2025Article
- Lanreotide protects against LPS-induced inflammation in endothelial cells and mouse lungs.Tissue barriers · 2025Article
- NEK2 inhibition alleviates lipopolysaccharide-induced endothelial injury.ASPET discovery · 2025Article
- Unfolded protein response modulates the effects of GHRH antagonists in experimental models ofTissue barriers · 2025Article
- Endothelial Unfolded Protein Response-Mediated Cytoskeletal Effects.Cell biochemistry and function · 2024Review
- Involvement of ATF6 in Octreotide-Induced Endothelial Barrier Enhancement.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Protective effects of growth hormone - releasing hormone antagonists in the lungs of septic mice.Cellular signalling · 2024Article
- Unfolded protein response suppression potentiates LPS-induced barrier dysfunction and inflammation in bovine pulmonary artery endothelial cells.Tissue barriers · 2024Article
- Involvement of NEK2 and NEK9 in LPS - induced endothelial barrier dysfunction.Microvascular research · 2024Article
- Growth hormone - releasing hormone in the context of inflammation and redox biology.Frontiers in immunology · 2024Article
- Article
- Ceapin-A7 potentiates lipopolysaccharide-induced endothelial injury.Journal of biochemical and molecular toxicology · 2023Article
- Fine particulate matter promotes airway inflammation and mucin production by activating endoplasmic reticulum stress and the IRE1α/NOD1/NF‑κB pathway.International journal of molecular medicine · 2023Article
- Divergent Proteome Reactivity Influences Arm-Selective Activation of the Unfolded Protein Response by Pharmacological Endoplasmic Reticulum Proteostasis Regulators.ACS chemical biology · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundEndothelial hyperpermeability is associated with sepsis and acute respiratory distress syndrome (ARDS). The identification of molecular pathways involved in barrier dysfunction; may reveal promising therapeutic targets to combat ARDS. Unfolded protein response (UPR) is a highly conserved molecular pathway, which ameliorates endoplasmic reticulum stress. The present work focuses on the effects of ATF6, which is a UPR sensor, in lipopolysaccharides (LPS)-induced endothelial hyperpermeability.
methodsThe in vitro effects of AA147 and Ceapin-A7 in LPS-induced endothelial barrier dysfunction were investigated in bovine pulmonary artery endothelial cells (BPAEC). Small interfering (si) RNA was utilized to "silence" ATF6, and electric cell-substrate impedance sensing (ECIS) measured transendothelial resistance. Fluorescein isothiocyanate (FITC)-dextran assay was utilized to assess paracellular permeability. Protein expression levels were evaluated with Western blotting, and cell viability with MTT assay.
resultsWe demonstrated that AA147 prevents LPS-induced barrier disruption by counteracting Cofilin and myosin light chain 2 (MLC2) activation, as well as VE-Cadherin phosphorylation. Moreover, this ATF6 inducer opposed LPS-triggered decrease in transendothelial resistance (TEER), as well as LPS-induced paracellular hyperpermeability. On the other hand, ATF6 suppression due to Ceapin-A7 or small interfering RNA exerted the opposite effects, and potentiated LPS-induced endothelial barrier disruption. Moderate concentrations of both ATF6 modulators did not affect cell viability.
conclusionsATF6 activation protects against endothelial barrier function, suggesting that this UPR sensor may serve as a therapeutic target for sepsis and ARDS.
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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.