ArticleMolecular medicine (Cambridge, Mass.)
Acute-phase protein α1-antitrypsin inhibits neutrophil calpain I and induces random migration.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 57 citations in OpenAlex.
- Neutrophil serine proteases degrade endothelial cortactin and promote extravasation.The Journal of cell biology · 2026Article
- Aqueous humor perturbations in chronic smokers: a proteomic study.Scientific reports · 2024Article
- Neutrophil-Derived Proteases in Lung Inflammation: Old Players and New Prospects.International journal of molecular sciences · 2024Review
- Role of Serine Protease Inhibitors A1 and A3 in Ocular Pathologies.Investigative ophthalmology & visual science · 2024Review
- A Review of Alpha-1 Antitrypsin Binding Partners for Immune Regulation and Potential Therapeutic Application.International journal of molecular sciences · 2022Review
- Application of alpha1-antitrypsin in a rat model of veno-arterial extracorporeal membrane oxygenation.Scientific reports · 2021Article
- Potential Roles of Acute Phase Proteins in Cancer: Why Do Cancer Cells Produce or Take Up Exogenous Acute Phase Protein Alpha1-Antitrypsin?Frontiers in oncology · 2021Review
- Exacerbations of Lung Disease in Alpha-1 Antitrypsin Deficiency.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2021Article
- Comprehensive Proteomic Profiling of Pressure Ulcers in Patients with Spinal Cord Injury Identifies a Specific Protein Pattern of Pathology.Advances in wound care · 2020Article
- Engineering the serpin αProtein science : a publication of the Protein Society · 2020Review
- Enhanced Survival and Accelerated Perfusion of Skin Flap to Recipient Site Following Administration of Human α1-Antitrypsin in Murine Models.Advances in wound care · 2019Article
- Preservation with αThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2018Article
- The Multifaceted Effects of Alpha1-Antitrypsin on Neutrophil Functions.Frontiers in pharmacology · 2018Review
- Article
- α-Linoleic acid enhances the capacity of α-1 antitrypsin to inhibit lipopolysaccharide induced IL-1β in human blood neutrophils.Molecular medicine (Cambridge, Mass.) · 2016Article
- Neutrophil Fates in Bronchiectasis and Alpha-1 Antitrypsin Deficiency.Annals of the American Thoracic Society · 2016Article
- Why do some adults with PiMZ α1-antitrypsin develop bronchiectasis? [corrected]ERJ open research · 2016Article
- Alpha-1 Antitrypsin Prevents the Development of Preeclampsia Through Suppression of Oxidative Stress.Frontiers in physiology · 2016Article
- COMP-Ang1 Potentiates EPC Treatment of Ischemic Brain Injury by Enhancing Angiogenesis Through Activating AKT-mTOR Pathway and Promoting Vascular Migration Through Activating Tie2-FAK Pathway.Experimental neurobiology · 2015Article
- Acute-phase protein α1-anti-trypsin: diverting injurious innate and adaptive immune responses from non-authentic threats.Clinical and experimental immunology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A rapid recruitment of neutrophils to sites of injury or infection is a hallmark of the inflammatory response and is required for effective host defense against pathogenic stimuli. However, neutrophil-mediated inflammation can also lead to chronic tissue destruction; therefore, a better understanding of the mechanisms underlying neutrophil influx and activation is of critical importance. We have previously shown that the acute phase protein α1-antitrypsin (AAT) inhibits neutrophil chemotaxis. In this study, we examine mechanisms related to the effect of AAT on neutrophil responses. We report a previously unknown function of AAT to inactivate calpain I (μ-calpain) and to induce a rapid cell polarization and random migration. These effects of AAT coincided with a transient rise in intracellular calcium, increase in intracellular lipids, activation of the Rho GTPases, Rac1 and Cdc42, and extra-cellular signal-regulated kinase (ERK1/2). Furthermore, AAT caused a significant inhibition of nonstimulated as well as formyl-met-leu-phe (fMLP)-stimulated neutrophil adhesion to fibronectin, strongly inhibited lipopolysaccharide-induced IL-8 release and slightly delayed neutrophil apoptosis. The results presented here broaden our understanding of the regulation of calpain-related neutrophil functional activities, and provide the impetus for new studies to define the role of AAT and other acute phase proteins in health and disease.
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