ArticleThe Journal of experimental medicine2009
Anaphylactic shock depends on endothelial Gq/G11.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 102 citations in OpenAlex.
- Phosphorylation of endothelial histone H3.3 serine 31 by PKN1 links flow-induced signaling to proatherogenic gene expression.Nature cardiovascular research · 2025Article
- Maternal supplementation with α-tocopherol inhibits the development of offspring food allergy, H1R signaling and ultimately anaphylaxis early in life.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Beyond genomic studies of congenital heart defects through systematic modelling and phenotyping.Disease models & mechanisms · 2024Article
- Studying the Pulmonary Endothelium in Health and Disease: An Official American Thoracic Society Workshop Report.American journal of respiratory cell and molecular biology · 2024Article
- GNAQ/GNA11 Mosaicism Causes Aberrant Calcium Signaling Susceptible to Targeted Therapeutics.The Journal of investigative dermatology · 2024Article
- Endothelial FAT1 inhibits angiogenesis by controlling YAP/TAZ protein degradation via E3 ligase MIB2.Nature communications · 2023Article
- Suppression of CCL2 angiocrine function by adrenomedullin promotes tumor growth.The Journal of experimental medicine · 2023Article
- Pathophysiological, Cellular, and Molecular Events of the Vascular System in Anaphylaxis.Frontiers in immunology · 2022Review
- Endothelial Cullin3 Mutation Impairs Nitric Oxide-Mediated Vasodilation and Promotes Salt-Induced Hypertension.Function (Oxford, England) · 2022Article
- Protein kinase N2 mediates flow-induced endothelial NOS activation and vascular tone regulation.The Journal of clinical investigation · 2021Article
- Mechanisms Governing Anaphylaxis: Inflammatory Cells, Mediators, Endothelial Gap Junctions and Beyond.International journal of molecular sciences · 2021Review
- Article
- Endothelial eNAMPT amplifies pre-clinical acute lung injury: efficacy of an eNAMPT-neutralising monoclonal antibody.The European respiratory journal · 2021Article
- Glycolysis is integral to histamine-induced endothelial hyperpermeability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Proteomic and Biological Analysis of anFrontiers in immunology · 2021Article
- Chronic activation of endothelial MAPK disrupts hematopoiesis via NFKB dependent inflammatory stress reversible by SCGF.Nature communications · 2020Article
- TAK1 regulates endothelial cell necroptosis and tumor metastasis.Cell death and differentiation · 2019Article
- Shear stress-induced endothelial adrenomedullin signaling regulates vascular tone and blood pressure.The Journal of clinical investigation · 2019Article
- Endothelial-Specific Cre Mouse Models.Arteriosclerosis, thrombosis, and vascular biology · 2018Review
- Piezo1 and GThe Journal of experimental medicine · 2018Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anaphylactic shock is a severe allergic reaction involving multiple organs including the bronchial and cardiovascular system. Most anaphylactic mediators, like platelet-activating factor (PAF), histamine, and others, act through G protein-coupled receptors, which are linked to the heterotrimeric G proteins G(q)/G(11), G(12)/G(13), and G(i). The role of downstream signaling pathways activated by anaphylactic mediators in defined organs during anaphylactic reactions is largely unknown. Using genetic mouse models that allow for the conditional abrogation of G(q)/G(11)- and G(12)/G(13)-mediated signaling pathways by inducible Cre/loxP-mediated mutagenesis in endothelial cells (ECs), we show that G(q)/G(11)-mediated signaling in ECs is required for the opening of the endothelial barrier and the stimulation of nitric oxide formation by various inflammatory mediators as well as by local anaphylaxis. The systemic effects of anaphylactic mediators like histamine and PAF, but not of bacterial lipopolysaccharide (LPS), are blunted in mice with endothelial G alpha(q)/G alpha(11) deficiency. Mice with endothelium-specific G alpha(q)/G alpha(11) deficiency, but not with G alpha(12)/G alpha(13) deficiency, are protected against the fatal consequences of passive and active systemic anaphylaxis. This identifies endothelial G(q)/G(11)-mediated signaling as a critical mediator of fatal systemic anaphylaxis and, hence, as a potential new target to prevent or treat anaphylactic reactions.
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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.