ArticleBlood advances2017
Loss of mDia1 causes neutropenia via attenuated CD11b endocytosis and increased neutrophil adhesion to the endothelium.
Article in Blood advances, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The trial behind it
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
10 citing papers in PubMed, 12 citations in OpenAlex.
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- Immune-related actinopathies at the cross-road of immunodeficiency, autoimmunity and autoinflammation.Nature reviews. Immunology · 2026Review
- ECRG4 mediates host response to cutaneous infection by regulating neutrophil recruitment and adhesion receptor expression.PloS one · 2024Article
- mDia formins form hetero-oligomers and cooperatively maintain murine hematopoiesis.PLoS genetics · 2023Article
- Article
- Diaphanous-related formin mDia2 regulates beta2 integrins to control hematopoietic stem and progenitor cell engraftment.Nature communications · 2020Article
- Protein diaphanous homolog 1 (Diaph1) promotes myofibroblastic activation of hepatic stellate cells by regulating Rab5a activity and TGFβ receptor endocytosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Mammalian diaphanous-related formin 1 (mDia1) coordinates mast cell migration and secretion through its actin-nucleating activity.The Journal of allergy and clinical immunology · 2019Article
- Recent Advances in Studies of Molecular Hydrogen against Sepsis.International journal of biological sciences · 2019Review
- Formin proteins in megakaryocytes and platelets: regulation of actin and microtubule dynamics.Platelets · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Formin protein mDia1 is involved in actin polymerization and plays important roles in the migration and adhesion of hematopoietic cells. The mDia1 encoding gene is located on chromosome 5q, which is commonly deleted in patients with del(5q) myelodysplastic syndromes (MDSs). We previously reported that mice with mDia1 deficiency developed neutropenia that closely mimics MDS. However, the mechanism of neutropenia in these mice and patients with del(5q) MDS remains incompletely defined. Here, we reveal that mDia1 knockout mice show cell-autonomously increased CD11b expression on neutrophils in the peripheral blood and bone marrow. The level of CD11b was also higher in patients with del(5q) MDS compared with normal individuals. Mechanistically, loss of mDia1 significantly attenuated the endocytosis of CD11b on neutrophils, which led to an increased number of neutrophils adhering to the blood vessels in mDia1 knockout mice. Administration of CD11b antibody to mDia1 knockout mice reduced the adhesion of neutrophils to the vessels and rescued neutropenia. Our study reveals the role of mDia1 deficiency in the upregulation of CD11b on neutrophils, which leads to their increased binding to the blood vessels. These results may provide important clues for the pathogenesis of neutropenia in patients with del(5q) MDS.
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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.