ArticleJournal of inflammation (London, England)2012
Cyclophilin A secreted from fibroblast-like synoviocytes is involved in the induction of CD147 expression in macrophages of mice with collagen-induced arthritis.
Article in Journal of inflammation (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Maternal Serum Cyclophilin A: A Predictive Biomarker of Preeclampsia in South Indian Women.Journal of obstetrics and gynaecology of India · 2025Article
- Extracellular and Intracellular Cyclophilin A, Native and Post-Translationally Modified, Show Diverse and Specific Pathological Roles in Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2018Review
- Composition of the Schistosoma mansoni worm secretome: Identification of immune modulatory Cyclophilin A.PLoS neglected tropical diseases · 2017Article
- Melittin inhibits the invasion of MCF-7 cells by downregulating CD147 and MMP-9 expression.Oncology letters · 2017Article
- Overexpression of aquaporin 4 in articular chondrocytes exacerbates the severity of adjuvant-induced arthritis in rats: anJournal of inflammation (London, England) · 2017Article
- Melatonin attenuates angiotensin II-induced cardiomyocyte hypertrophy through the CyPA/CD147 signaling pathway.Molecular and cellular biochemistry · 2016Article
- Extracellular cyclophilins in health and disease.Biochimica et biophysica acta · 2015Review
- Expression of hedgehog signal pathway in articular cartilage is associated with the severity of cartilage damage in rats with adjuvant-induced arthritis.Journal of inflammation (London, England) · 2015Article
- The biological function and clinical utilization of CD147 in human diseases: a review of the current scientific literature.International journal of molecular sciences · 2014Review
- Acetylation of cyclophilin A is required for its secretion and vascular cell activation.Cardiovascular research · 2014Article
- Inhibition of synovitis and joint destruction by a new single domain antibody specific for cyclophilin A in two different mouse models of rheumatoid arthritis.Arthritis research & therapy · 2013Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelled
backgroundCyclophilin A (CypA), a member of the immunophilin family, is a ubiquitously distributed intracellular protein. Recent studies have shown that CypA is secreted by cells in response to inflammatory stimuli. Elevated levels of extracellular CypA and its receptor, CD147 have been detected in the synovium of patients with RA. However, the precise process of interaction between CypA and CD147 in the development of RA remains unclear. This study aimed to investigate CypA secretion from fibroblast-like synoviocytes (FLS) isolated from mice with collagen-induced arthritis (CIA) and CypA-induced CD147 expression in mouse macrophages.
findingsCIA was induced by immunization with type II collagen in mice. The expression and localization of CypA and CD147 was investigated by immunoblotting and immunostaining. Both CypA and CD147 were highly expressed in the joints of CIA mice. CD147 was expressed in the infiltrated macrophages in the synovium of CIA mice. In vitro, spontaneous CypA secretion from FLS was detected and this secretion was increased by stimulation with lipopolysaccharide. CypA markedly increased CD147 levels in macrophages.
conclusionsThese findings suggest that an interaction in the synovial joints between extracellular CypA and CD147 expressed by macrophages may be involved in the mechanisms underlying the development of arthritis.
Identifiers
What OpenQuestion holds
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.