ArticleThe American journal of pathology2018
Serum Amyloid A1 Is an Epithelial Prorestitutive Factor.
Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 23 citations in OpenAlex.
- Diverse infections transcriptionally reprogram the intestinal epithelium and epithelial-immune cell interactions.Nature immunology · 2026Article
- Single-cell analysis reveals that the hormone T3 affects colon epithelial differentiation and induces a mixed progenitor-like cell population.Scientific reports · 2026Article
- Recent Advances in Studies of Serum Amyloid A: Implications in Inflammation, Immunity and Tumor Metastasis.International journal of molecular sciences · 2025Review
- TheFrontiers in immunology · 2025Review
- Analysis of blood proteome in influenza-infected patients reveals new insights into the host response signatures distinguishing mild severe infections.Frontiers in immunology · 2025Article
- Neutrophil-activating secretome characterizes palbociclib-induced senescence of breast cancer cells.Cancer immunology, immunotherapy : CII · 2024Article
- Single-cell analysis of endometriosis reveals a coordinated transcriptional programme driving immunotolerance and angiogenesis across eutopic and ectopic tissues.Nature cell biology · 2022Article
- The Role of Formyl Peptide Receptors in Permanent and Low-Grade Inflammation:International journal of molecular sciences · 2021Review
- The Role of Formyl Peptide Receptors in Neurological Diseases via Regulating Inflammation.Frontiers in cellular neuroscience · 2021Review
- Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity.Nature immunology · 2020Article
- Soluble pattern recognition molecules: Guardians and regulators of homeostasis at airway mucosal surfaces.European journal of immunology · 2020Review
- Innate immune cell-epithelial crosstalk during wound repair.The Journal of clinical investigation · 2019Review
- Chemotactic Ligands that Activate G-Protein-Coupled Formylpeptide Receptors.International journal of molecular sciences · 2019Review
- Silencing of SAA1 inhibits palmitate- or high-fat diet induced insulin resistance through suppression of the NF-κB pathway.Molecular medicine (Cambridge, Mass.) · 2019Article
- Contribution of Wound-Associated Cells and Mediators in Orchestrating Gastrointestinal Mucosal Wound Repair.Annual review of physiology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Several proteins endogenously produced during the process of intestinal wound healing have demonstrated prorestitutive properties. The presence of serum amyloid A1 (SAA1), an acute-phase reactant, within inflamed tissues, where it exerts chemotaxis of phagocytes, is well recognized; however, a putative role in intestinal wound repair has not been described. Herein, we show that SAA1 induces intestinal epithelial cell migration, spreading, and attachment through a formyl peptide receptor 2-dependent mechanism. Induction of the prorestitutive phenotype is concentration and time dependent and is associated with epithelial reactive oxygen species production and alterations in p130 Crk-associated substrate staining. In addition, using a murine model of wound recovery, we provide evidence that SAA1 is dynamically and temporally regulated, and that the elaboration of SAA1 within the wound microenvironment correlates with the influx of SAA1/CD11b coexpressing immune cells and increases in cytokines known to induce SAA expression. Overall, the present work demonstrates an important role for SAA in epithelial wound recovery and provides evidence for a physiological role in the wound environment.
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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.