ArticleAnnals of translational medicine2020
Class A1 scavenger receptors mediated macrophages in impaired intestinal barrier of inflammatory bowel disease.
Article in Annals of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- LncRNA MNX1-AS1 drives the progression of non-small cell lung cancer and serves as a ceRNA to target COMMD8 by sponging miR-218-5p.Journal of molecular histology · 2026Article
- Class A1 scavenger receptor antibody improves murine colitis by influencing macrophage and gut microbiota.Scientific reports · 2024Article
- MicroRNA-218-5p accelerates malignant behaviors of breast cancer through LRIG1.Clinics (Sao Paulo, Brazil) · 2024Article
- Damage-mediated macrophage polarization in sterile inflammation.Frontiers in immunology · 2023Review
- Bacterial Cellulose as a Potential Bio-Scaffold for Effective Re-Epithelialization Therapy.Pharmaceutics · 2021Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was to investigate the cytokines and phenotype of macrophages pre-treated with class A1 scavenger receptor (SR-A1) antibody in vitro and the influence on apoptotic pathway of colonic epithelial cells, and to explore the role of SR-A1 mediated macrophages in impaired intestinal barrier of inflammatory bowel diseases (IBDs).
methodsMouse macrophage RAW264.7 was pre-treated with SR-A1 antibody in the presence of lipopolysaccharide (LPS). Transwell system was employed for co-culture of RAW264.7 and Caco-2 in the presence of LPS and IFN-γ, with or without SR-A1 antibody pre-treatment. The percentage of F4/80
resultsPre-treatment with SR-A1 antibody up-regulated IL-10 expression in RAW264.7, whereas down-regulated the expression of TNF and iNOS. Immunofluorescence staining indicated the upregulation of NF-κB p-p56 after LPS stimulation was significantly inhibited in the presence of SR-A1 antibody. The increase in p-JNK expression was inhibited by SR-A1 antibody. Transwell assay showed the percentage of F4/80
conclusionsPre-treatment with SR-A1 antibody can inhibit inflammatory response in LPS-induced macrophages in a NF-κB dependent manner. Pre-treatment with SR-A1 antibody also inhibits M1 phenotype expression of macrophages, and attenuates the pro-apoptotic effect on colonic epithelial cells and disruption of intestinal barrier integrity induced by macrophages.
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