ArticleEBioMedicine2019
Osteoblastic PLEKHO1 contributes to joint inflammation in rheumatoid arthritis.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- LncRNA MIAT inhibits osteoblast differentiation and function in rheumatoid arthritis via let-7i-5p/ CKIP-1 axis.Arthritis research & therapy · 2026Article
- Research progress of SIRTs activator resveratrol and its derivatives in autoimmune diseases.Frontiers in immunology · 2024Review
- Sirtuin 6 ameliorates arthritis through modulating cyclic AMP-responsive element binding protein/CCN1/cyclooxygenase 2 pathway in osteoblasts.Journal of bone and mineral metabolism · 2023Article
- PDCD5 as a Potential Biomarker for Improved Prediction of the Incidence and Remission for Patients with Rheumatoid Arthritis.Rheumatology and therapy · 2023Article
- Noninvasive Imaging OX40Molecular imaging and biology · 2023Article
- Mechanisms of joint destruction in rheumatoid arthritis - immune cell-fibroblast-bone interactions.Nature reviews. Rheumatology · 2022Review
- Osteoblast role in the pathogenesis of rheumatoid arthritis.Molecular biology reports · 2021Review
- Hepatocyte growth factor overexpression promotes osteoclastogenesis and exacerbates bone loss in CIA mice.Journal of orthopaedic translation · 2021Article
- Epigenome wide association study of response to methotrexate in early rheumatoid arthritis patients.PloS one · 2021Article
- An immune-related signature that to improve prognosis prediction of breast cancer.American journal of cancer research · 2021Article
- Comprehensive Analysis of Common Different Gene Expression Signatures in the Neutrophils of Sepsis.BioMed research international · 2021Article
- Pleckstrin Levels Are Increased in Patients with Chronic Periodontitis and RegulatedFrontiers in immunology · 2021Article
- Roles of MicroRNAs in Bone Destruction of Rheumatoid Arthritis.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOsteoblasts participating in the inflammation regulation gradually obtain concerns. However, its role in joint inflammation of rheumatoid arthritis (RA) is largely unknown. Here, we investigated the role of osteoblastic pleckstrin homology domain-containing family O member 1 (PLEKHO1), a negative regulator of osteogenic lineage activity, in regulating joint inflammation in RA.
methodsThe level of osteoblastic PLEKHO1 in RA patients and collagen-induced arthritis (CIA) mice was examined. The role of osteoblastic PLEKHO1 in joint inflammation was evaluated by a CIA model and a K/BxN serum-transfer arthritis (STA) model which were induced in osteoblast-specific Plekho1 conditional knockout mice and mice expressing high Plekho1 exclusively in osteoblasts, respectively. The effect of osteoblastic PLEKHO1 inhibition was explored in a CIA mice model and a non-human primate arthritis model. The mechanism of osteoblastic PLEKHO1 in regulating joint inflammation were performed by a series of in vitro studies.
resultsPLEKHO1 was highly expressed in osteoblasts from RA patients and CIA mice. Osteoblastic Plekho1 deletion ameliorated joint inflammation, whereas overexpressing Plekho1 only within osteoblasts exacerbated local inflammation in CIA mice and STA mice. PLEKHO1 was required for TRAF2-mediated RIP1 ubiquitination to activate NF-κB for inducing inflammatory cytokines production in osteoblasts. Moreover, osteoblastic PLEKHO1 inhibition diminished joint inflammation and promoted bone formation in CIA mice and non-human primate arthritis model.
conclusionsThese data strongly suggest that the highly expressed PLEKHO1 in osteoblasts contributes to joint inflammation in RA. Targeting osteoblastic PLEKHO1 may exert dual therapeutic action of alleviating joint inflammation and promoting bone formation in RA.
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