ArticleProceedings of the National Academy of Sciences of the United States of America1991
Transforming growth factor beta 1, a potent chemoattractant for human neutrophils, bypasses classic signal-transduction pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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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
66 citing papers in PubMed, 222 citations in OpenAlex.
- TGF-β signalling drives chemotaxis of human induced pluripotent stem cell-derived cardiomyocytes in response to MI stimulus.Basic research in cardiology · 2026Article
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- Age-dependent immune responses and resident cell dynamics in young mice following pneumonia.iScience · 2026Article
- Transforming Growth Factor-β1 Drives Neutrophil Chemokinesis, Not Chemotaxis.Journal of inflammation research · 2026Article
- Psychological stress increases skin infection through the action of TGFβ to suppress immune-acting fibroblasts.Science immunology · 2025Article
- Plasticity and Tumor Microenvironment in Pancreatic Cancer: Genetic, Metabolic, and Immune Perspectives.Cancers · 2024Review
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- Role of Elevated Serum TGF-β1 and the Common PromoterMedicina (Kaunas, Lithuania) · 2024Article
- Investigating the role of platelets and platelet-derived transforming growth factor-β in idiopathic pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- 3D-Printed Functional Hydrogel by DNA-Induced Biomineralization for Accelerated Diabetic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Ghrelin Modulates Differential Expression of Genes Relevant to Immune Activities and Antimicrobial Peptides in Primary Head Kidney Cells of Rainbow Trout (Animals : an open access journal from MDPI · 2023Article
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- Acute Inflammation in Tissue Healing.International journal of molecular sciences · 2022Review
- Macrophage TGF-β signaling is critical for wound healing with heterotopic ossification after trauma.JCI insight · 2022Article
- Neutrophil and natural killer cell imbalances prevent muscle stem cell-mediated regeneration following murine volumetric muscle loss.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Lack ofeLife · 2022Article
- Macrophage and Neutrophil Interactions in the Pancreatic Tumor Microenvironment Drive the Pathogenesis of Pancreatic Cancer.Cancers · 2021Review
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- Hyperosmolarity benefits cartilage regeneration by enhancing expression of chondrogenic markers and reducing inflammatory markers.In vitro cellular & developmental biology. Animal · 2021Article
- On Deep Landscape Exploration of COVID-19 Patients Cells and Severity Markers.Frontiers in immunology · 2021Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor beta 1 (TGF-beta 1), a homodimeric polypeptide (Mr 25,000), derives from inflammatory cells and acts as a chemoattractant for monocytes and fibroblasts. We report here that TGF-beta 1 is also the most potent chemoattractant yet described for human peripheral blood neutrophils. Recombinant TGF-beta 1 elicited dose-dependent directed migration of neutrophils under agarose that was inhibited in the presence of a neutralizing antibody to TGF-beta 1. Maximal chemotaxis was evoked by TGF-beta 1 at femtomolar concentrations, whereas conventional chemoattractants act at nanomolar concentrations: on a molar basis, TGF-beta 1 was 150,000 times more potent than fMet-Leu-Phe. In contrast, TGF-beta 1 provoked neither exocytosis nor the production of superoxide by neutrophils. We further analyzed the mechanism by which TGF-beta 1 elicits chemotaxis (GTPase activity, [Ca2+], and actin polymerization). In contrast to the conventional chemoattractant fMet-Leu-Phe, TGF-beta neither activated classic heterotrimeric guanine nucleotide-binding proteins nor provoked global mobilization of intracellular Ca2+. Chemoattraction by both fMet-Leu-Phe and TGF-beta 1 was inhibited by cycloheximide and actinomycin D. Moreover, chemotaxis in response to TGF-beta 1 was associated with the polymerization of actin. The selectivity and potency of TGF-beta 1 as a chemoattractant suggest that it elicits directed cell migration by means of a pathway that depends not on classic intracellular signals but on protein synthesis.
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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.