ArticleThe American journal of pathology2010
Silencing the expression of Ras family GTPase homologues decreases inflammation and joint destruction in experimental arthritis.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Elucidating Ras protein as a dual therapeutic target for inflammation and cancer: a review.Discover oncology · 2025Review
- Mechanism of Asperosaponin VI Related to EGFR/MMP9/AKT/PI3K Pathway in Treatment of Rheumtoid Arthritis.Chinese journal of integrative medicine · 2025Article
- High Humidity Alters Myeloid-Derived Suppressor Cells in Spleen Tissue: Insights into Rheumatoid Arthritis Progression.Journal of inflammation research · 2024Article
- Berberine inhibits RA-FLS cell proliferation and adhesion by regulating RAS/MAPK/FOXO/HIF-1 signal pathway in the treatment of rheumatoid arthritis.Bone & joint research · 2023Article
- MicroRNA-133 suppresses cell viability and migration of rheumatoid arthritis fibroblast-like synoviocytes by down-regulation of MET, EGFR, and FSCN1 expression.Molecular and cellular biochemistry · 2022Article
- Wutou decoction attenuates rheumatoid arthritis by modulating the Ahr/LOC101928120/SHC1 pathway.Pharmaceutical biology · 2021Article
- Glycolysis Rate-Limiting Enzymes: Novel Potential Regulators of Rheumatoid Arthritis Pathogenesis.Frontiers in immunology · 2021Review
- An anionic phthalocyanine decreases NRAS expression by breaking down its RNA G-quadruplex.Nature communications · 2018Article
- Mesenchymal stem cell-derived inflammatory fibroblasts promote monocyte transition into myeloid fibroblasts via an IL-6-dependent mechanism in the aging mouse heart.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling.Carcinogenesis · 2015Review
- Inhibitory effects of H-Ras/Raf-1-binding affibody molecules on synovial cell function.AMB Express · 2014Article
- Macrophages in multiple myeloma: emerging concepts and therapeutic implications.Leukemia & lymphoma · 2013Review
- Combined point mutations in codon 12 and 13 of KRAS oncogene in prostate carcinomas.Molecular biology reports · 2012Article
- Signal transduction pathways in chronic inflammatory autoimmune disease: small GTPases.The open rheumatology journal · 2012Article
- Does Harvey-Ras gene expression lead to oral squamous cell carcinoma? A clinicopathological aspect.Journal of oral and maxillofacial pathology : JOMFPArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 1 institution in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in the expression and activation status of Ras proteins are thought to contribute to the pathological phenotype of stromal fibroblast-like synoviocytes (FLS) in rheumatoid arthritis, a prototypical immune-mediated inflammatory disease. Broad inhibition of Ras and related proteins has shown protective effects in animal models of arthritis, but each of the Ras family homologues (ie, H-, K-, and N-Ras) makes distinct contributions to cellular activation. We examined the expression of each Ras protein in synovial tissue and FLS obtained from patients with rheumatoid arthritis and other forms of inflammatory arthritis. Each Ras protein was expressed in synovial tissue and cultured FLS. Each homolog was also activated following FLS stimulation with tumor necrosis factor-α or interleukin (IL)-1β. Constitutively active mutants of each Ras protein enhanced IL-1β-induced FLS matrix metalloproteinase-3 production, while only active H-Ras enhanced IL-8 production. Gene silencing demonstrated that each Ras protein contributed to IL-1β-dependent IL-6 production, while H-Ras and N-Ras supported IL-1β-dependent matrix metalloproteinase-3 and IL-8 production, respectively. The overlap in contributions of Ras homologues to FLS activation suggests that broad targeting of Ras GTPases in vivo suppresses global inflammation and joint destruction in arthritis. Consistent with this, simultaneous silencing of H-Ras, K-Ras, and N-Ras expression significantly reduces inflammation and joint destruction in murine collagen-induced arthritis, while specific targeting of N-Ras alone is less effective in providing clinical benefits.
Indexed as
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.