ArticleClinical and experimental medicine2011
β1,4-galactosyltransferase-I in synovial tissue of collagen-induced rat model of rheumatoid arthritis.
Article in Clinical and experimental medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- MicroRNA-15a/β1,4-GalT-I axis contributes to cartilage degeneration via NF-κB signaling in osteoarthritis.Clinics (Sao Paulo, Brazil) · 2023Article
- The Number of Regulatory B Cells is Increased in Mice with Collagen-induced Arthritis.Open life sciences · 2019Article
- Elevated expression of β1,4-galactosyltransferase-I in cartilage and synovial tissue of patients with osteoarthritis.Inflammation · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β1,4-galactosyltransferase-I (β1,4-GalT-I), which is one of the best-studied glycosyltransferases, plays a key role in the synthesis of selectin ligands such as sialyl Lewis (sLe(x)) and sulfated sLe(x). Previous studies showed that inflammatory responses of β1,4-GalT-I-deficient mice were impaired because of the defect in selectin-ligand biosynthesis. However, the expression of β1,4-GalT-I and its biological function in rheumatoid arthritis (RA) remain to be elucidated. The mRNA and protein expression of β1,4-GalT-I increased in synovial tissue of the RA group compared with the Normal group at 10d and 15d after collagen-induced. Double staining indicated β1,4-GalT-I overlapped with macrophage-like synoviocytes (MLSs), fibroblast-like synoviocytes (FLSs), neutrophils and tumor necrosis factor-α (TNF-α). Moreover, β1,4-GalT-I mRNA in FLSs in vitro was affected in a dose- and time-dependent manner in response to TNF-α stimulation. ELISA revealed that expression of TNF-α was attenuated in FLSs in vitro treated with β1,4-GalT-I-Ab. We therefore suggest that β1,4-GalT-I may play an important role in the inflammation process of RA synovial tissue, which would provide the foundation for further researching into the concrete mechanism of β1,4-GalT-I in RA.
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