ArticlePloS one2022
Promoting mechanism of serum amyloid a family expression in mouse intestinal epithelial cells.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- IL-22 increases proglucagon-expressing enteroendocrine cells via STAT3 in human iPSC-derived intestinal epithelium.Endocrinology · 2026Article
- SAA1 Promotes Ulcerative Colitis and Activating Colonic TLR4/NF-κB/NLRP3 Signaling Pathway.Inflammation · 2025Article
- Balancing inflammation: the specific roles of serum amyloid A proteins in sterile and infectious diseases.Frontiers in immunology · 2025Article
- Sodium oligomannate disrupts the adherence of RibCell discovery · 2024Article
- Real-Time 3D Imaging and Inhibition Analysis of Human Serum Amyloid A Aggregations Using Quantum Dots.International journal of molecular sciences · 2024Article
- Serum amyloid protein A in inflammatory bowel disease: from bench to bedside.Cell death discovery · 2023Review
- Comprehensive transcriptome profiling of urothelial cells following TNFα stimulation in anFrontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serum amyloid A (SAA) is an acute phase inflammatory protein that we previously described as a robust biomarker of colorectal inflammation in patients with ulcerative colitis (UC) in clinical remission. However, what induces SAA expression in UC remains unclear. This study demonstrates that SAA is significantly expressed in the intestinal tract of UC mouse models when compared with C-reactive protein, another inflammatory biomarker. Moreover, interleukin-6 and tumor necrosis factor-α were found to promote SAA1 expression, as were Toll-like receptor ligands flagellin and lipopolysaccharide. Furthermore, results suggested that the nuclear factor-kappa B (NF-κB) pathway may be involved in the promotion of SAA1 expression by flagellin, which was inhibited by treatment with 5-aminosalicylic acid (5-ASA). Therefore, the flagellin/NF-κB/SAA1 axis may represent one of the mechanisms by which 5-ASA suppresses intestinal inflammation.
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Registered trials
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