ArticleProceedings of the National Academy of Sciences of the United States of America2015
Platelet Gi protein Gαi2 is an essential mediator of thrombo-inflammatory organ damage in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 44 citations in OpenAlex.
- Gαi1/3 Is a Novel Regulatory Target for RANKL Signal Transduction and Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- GαInternational journal of molecular sciences · 2025Article
- Proteomic profiling of the local and systemic immune response to pediatric respiratory viral infections.mSystems · 2025Article
- Targeting GαBasic research in cardiology · 2024Article
- How Protein Depletion Balances Thrombosis and Bleeding Risk in the Context of Platelet's Activatory and Negative Signaling.International journal of molecular sciences · 2024Review
- MiR-30c-5p-Targeted Regulation of GNAI2 Improves Neural Function Injury and Inflammation in Cerebral Ischemia-Reperfusion Injury.Applied biochemistry and biotechnology · 2024Article
- Roles of G proteins and their GTPase-activating proteins in platelets.Bioscience reports · 2024Review
- Protective effects of GαNaunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Cerebrovascular GMolecular imaging and biology · 2023Article
- Data on common carotid artery occlusion inducing focalized stroke lesions after Pertussis toxin injection.Data in brief · 2023Article
- Article
- Analyses of Gnai3-iresGFP reporter mice reveal unknown GαScientific reports · 2021Article
- A novel technique for laser-assisted revascularization: an in vitro pilot study.Lasers in medical science · 2021Article
- The effect of platelet G proteins on platelet extravasation and tumor growth in the murine model of ovarian cancer.Blood advances · 2021Article
- Platelets as drivers of ischemia/reperfusion injury after stroke.Blood advances · 2021Review
- Selective protection of murine cerebral GJournal of molecular medicine (Berlin, Germany) · 2020Article
- Function, Regulation and Biological Roles of PI3Kγ Variants.Biomolecules · 2019Review
- Deletion of the α subunit of the heterotrimeric Go protein impairs cerebellar cortical development in mice.Molecular brain · 2019Article
- Platelets Are at the Nexus of Vascular Diseases.Frontiers in cardiovascular medicine · 2019Review
- Platelet Contributions to Myocardial Ischemia/Reperfusion Injury.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
Platelets are crucial for hemostasis and thrombosis and exacerbate tissue injury following ischemia and reperfusion. Important regulators of platelet function are G proteins controlled by seven transmembrane receptors. The Gi protein Gα(i2) mediates platelet activation in vitro, but its in vivo role in hemostasis, arterial thrombosis, and postischemic infarct progression remains to be determined. Here we show that mice lacking Gα(i2) exhibit prolonged tail-bleeding times and markedly impaired thrombus formation and stability in different models of arterial thrombosis. We thus generated mice selectively lacking Gα(i2) in megakaryocytes and platelets (Gna(i2)(fl/fl)/PF4-Cre mice) and found bleeding defects comparable to those in global Gα(i2)-deficient mice. To examine the impact of platelet Gα(i2) in postischemic thrombo-inflammatory infarct progression, Gna(i2)(fl/fl)/PF4-Cre mice were subjected to experimental models of cerebral and myocardial ischemia/reperfusion injury. In the model of transient middle cerebral artery occlusion stroke Gna(i2)(fl/fl)/PF4-Cre mice developed significantly smaller brain infarcts and fewer neurological deficits than littermate controls. Following myocardial ischemia, Gna(i2)(fl/fl)/PF4-Cre mice showed dramatically reduced reperfusion injury which correlated with diminished formation of the ADP-dependent platelet neutrophil complex. In conclusion, our data provide definitive evidence that platelet Gα(i2) not only controls hemostatic and thrombotic responses but also is critical for the development of ischemia/reperfusion injury in vivo.
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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.