ArticleInflammation2011
Tumor necrosis factor-α up-regulates the expression of β1,4-galactosyltransferase-I in human fibroblast-like synoviocytes.
Article in Inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Immune regulatory networks coordinated by glycans and glycan-binding proteins in autoimmunity and infection.Cellular & molecular immunology · 2023Review
- Glycobiology of rheumatic diseases.Nature reviews. Rheumatology · 2023Review
- Loss of α2-6 sialylation promotes the transformation of synovial fibroblasts into a pro-inflammatory phenotype in arthritis.Nature communications · 2021Article
- β1,4-galactosyltransferase-I protects chondrocytes against TNF-induced apoptosis by blocking the TLR4 signaling pathway.American journal of translational research · 2019Article
- Mice overexpressing β-1,4-Galactosyltransferase I are resistant to TNF-induced inflammation and DSS-induced colitis.PloS one · 2013Article
- Elevated expression of β1,4-galactosyltransferase-I in cartilage and synovial tissue of patients with osteoarthritis.Inflammation · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β1,4-Galactosyltransferase-I (β1,4-GalT-I), which transfers galactose to the terminal N-acetylglucosamine of N- and O-linked glycans in a β1,4-linkage, is considered to be the major galactosyltransferase among the seven members of the subfamily responsible for β4 galactosylation. We previously reported, for the first time, that β1,4-GalT-I may play an important role in the inflammatory processes in synovial tissue of patients with rheumatoid arthritis (RA). In this study, we analyzed whether β1,4-GalT-I expression correlates with the expression of tumor necrosis factor-α (TNF-α) in RA. We show firstly the overexpression and co-localization of β1,4-GalT-I and TNF-α in synovial tissue of RA patients. Then, lipopolysaccharide (LPS) induces β1,4-GalT-I mRNA up-regulation in fibroblast-like synoviocytes (FLSs) through endogenous TNF-α overexpression. In addition, we observed that not only endogenous TNF-α but also exogenous TNF-α induced β1,4-GalT-I mRNA production in FLSs, and TNF-α-knockdown reverses the up-regulation of β1,4-GalT-I in FLSs induced by LPS or TNF-α. These results suggest that TNF-α contributes to the up-regulation of β1,4-GalT-I mRNA in human FLSs.
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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.