ArticleThe Journal of veterinary medical science2014
Up-regulation of MUC2 mucin expression by serum amyloid A3 protein in mouse colonic epithelial cells.
Article in The Journal of veterinary medical science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- The role of glycosylated mucins in maintaining intestinal homeostasis and gut health.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Review
- Blocking MyD88 signaling with MyD88 inhibitor prevents colitis-associated colorectal cancer development by maintaining colonic microbiota homeostasis.Scientific reports · 2023Article
- Intestinal mucus components and secretion mechanisms: what we do and do not know.Experimental & molecular medicine · 2023Review
- Integrative analyses of mRNA and microRNA expression profiles reveal the innate immune mechanism for the resistance toFrontiers in immunology · 2022Article
- Induction of Serum Amyloid A3 in Mouse Mammary Epithelial Cells Stimulated with Lipopolysaccharide and Lipoteichoic Acid.Animals : an open access journal from MDPI · 2021Article
- Differential expression of serum amyloid A1 and A3 in bovine epithelia.The Journal of veterinary medical science · 2020Article
- Biological Characterization of Commercial Recombinantly Expressed Immunomodulating Proteins Contaminated with Bacterial Products in the Year 2020: The SAA3 Case.Mediators of inflammation · 2020Article
- Lipopolysaccharide and lipoteichoic acid enhance serum amyloid A3 mRNA expression in murine alveolar epithelial cells.The Journal of veterinary medical science · 2019Article
- Article
- Emerging functions of serum amyloid A in inflammation.Journal of leukocyte biology · 2015Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Serum amyloid A (SAA) proteins are acute-phase proteins and are classified into multiple isoforms; however, the biological functions of each SAA isoform are not fully understood. In this study, to clarify the roles of SAA3 in the intestine, we characterized mRNA expression in mouse colonic epithelial CMT-93 cells treated with rotavirus, Toxoplasma, Staphylococcus aureus, and Escherichia coli, as well as lipopolysaccharide (LPS) and recombinant murine SAAs (rSAAs). E. coli together with LPS, but not the other pathogens, enhanced SAA3 mRNA expression. The mRNA expression of SAA3 by dead E. coli was higher than that by living E. coli, and the mRNA expression by E. coli and LPS increased in a dose-dependent manner. In contrast, mRNA expressions of SAA1 and/or SAA2 were not stimulated by any of the treatments. In comparisons of cell treatments with rSAA1 or rSAA3, rSAA3 significantly up-regulated the mRNA expression of mucin 2 (MUC2), a major component of the mucus layer of the intestines that acts as an epithelial cell barrier against pathogens, while MUC2 mRNA expression was not significantly increased by E. coli and LPS. Furthermore, treatment with rSAAs intensively induced tumor necrosis factor-α mRNA expression. These results suggest that SAA3 plays a role in host innate immunity in the colon by up-regulating MUC2 mucin production, which builds a physiological barrier of colonic epithelia against bacterial invasion.
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