Effects of relaxin and estrogens on bone remodeling markers, receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG), in rat adjuvant-induced arthritis

Ho, Teh‐Yuan; Santora, Karen; Chen, Joseph C.; Frankshun, Amy-Lynn; Bagnell, Carol A.

doi:10.1016/j.bone.2011.03.684

Cited by 45 publications

(36 citation statements)

References 41 publications

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“…11 Studies suggest that estrogen can modulate the RANKL-OPG system and increase levels of OPG, causing a decrease in the RANKL/OPG protein ratio. 12,13 Under certain circumstances, disequilibrium in the RANK/RANKL/OPG triad induces an enhanced activity of osteoclasts assessed by an increase in tartrate-resistant acid-phosphatase (TRAP) staining. 14,15 Because multinuclear TRAP-positive cells resorb bone, TRAP is a specific osteoclast differentiation marker.…”

mentioning

confidence: 99%

Adjunctive Antimicrobial Photodynamic Treatment of Experimentally Induced Periodontitis in Rats With Ovariectomy

Garcia

Júnior

Fernandes

et al. 2013

Journal of Periodontology

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confidence: 99%

Adjunctive Antimicrobial Photodynamic Treatment of Experimentally Induced Periodontitis in Rats With Ovariectomy

Garcia

Júnior

Fernandes

et al. 2013

Journal of Periodontology

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“…RANKL belongs to the tumor necrosis factor superfamily, acting as a ligand for the receptors RANK and OPG (37). RANK is located on the plasma membrane of osteoclast precursor cells, and the binding of RANKL to RANK promotes the differentiation and maturity of osteoclasts (38). The binding capacity of OPG to RANKL is higher than that of RANK to RANKL, which competitively binds RANKL, thereby competitively inhibiting its binding to RANK (39).…”

mentioning

confidence: 99%

(5R)-5-hydroxytriptolide (LLDT-8) prevents collagen-induced arthritis through OPG/RANK/RANKL signaling in a rat model of rheumatoid arthritis

Zeng

Meng

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. (5R)-5-hydroxytriptolide (LLDT-8) extracts fromTripterygium have anti-inflammatory, antineoplastic and immunity adjustment functions. The present study used a collagen-induced arthritis (CIA) model to evaluate whether LLDT-8 prevents collagen-induced arthritis, and investigated the signaling underlying this. Male Sprague-Dawley rats were induced to generate CIA, mimicking rheumatoid arthritis (RA). The presence of arthritis was determined using RA progression scores. The inflammatory cytokines interleukin (IL)-1β, IL-6 and nuclear factor-κB were detected using enzyme-linked immunosorbent assay kits. Induced nitric oxide synthase (iNOS) and matrix metalloprotease (MMP)-13 protein expression were measured using western blot analysis. Lastly, reverse transcription-quantitative polymerase chain reaction was used to evaluate osteoprotegerin (OPG) and receptor activator of nuclear factor κB (RANK) gene expression. LLDT-8 improved RA progression scores and reduced the incidence and severity of CIA. Furthermore, LLDT-8 administration inhibited collagen-induced inflammation and iNOS protein expression in arthritic rats. The current data indicated that MMP-13 production was suppressed and OPG/RANKL expression was increased by LLDT-8 treatment in the arthritic rat. The present results suggest that LLDT-8 attenuates CIA through OPG/RANK/RANK ligand signaling in a rat model of RA. IntroductionRheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that is characterized by erosive arthrosynovitis (1).The incidence of RA in females is more than that in males, at a ratio of 1:3 (2). The mortality rate of RA in worldwide populations varies from 0.01-0.05%, and prevalence rate is 0.18-1.07% (3). RA is also an impactful disease, resulting in labor loss and disability in China (2). According to US epidemiological investigation over the last 40 years, the difference in mortality rate between RA patients and the general population has increased (4). The risk of cognitive impairment for RA patients is higher than that of the general population (5). The etiology of RA is unclear. Previous studies suggest that RA is associated with genetic factors, infection, immunity and endocrine function (6,7).The main pathological characteristics of RA are hyperplasia of synovial cells and T cell accumulation during inflammation of synovial tissues, accompanied by pannus formation, followed by damage to the cartilage and bone (8). Finally, RA causes joint deformity and functional loss (9). These pathological changes may result from a combination of genetic mutations, activation of protooncogenes, lesions of synoviocytes, release of proinflammatory cytokines by inflammatory cells during infiltration of synovial tissues, chemotactic factors and enzymatic degradation of stromal proteins, amongst other factors (10). The etiology of RA is unclear, but it is universally believed to be a multifactorial disease, associated with genetic, environmental and infective factors (11). Autoimmunity may arise due to genetic factors, or as an ab...

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“…34 Additionally, higher RANKL/OPG ratios were found in some inflamed tissues. 35 To our knowledge, OPG acts as a decoy receptor, binding to RANKL, preventing the interaction between RANK and RANKL. 7 Therefore OPG appears to have 2 different roles in this scenario.…”

Section: Discussionmentioning

confidence: 99%

Dysregulated Atrial Gene Expression of Osteoprotegerin/Receptor Activator of Nuclear Factor-.KAPPA.B (RANK)/RANK Ligand Axis in the Development and Progression of Atrial Fibrillation

Cao

Wang

Liu

et al. 2011

Circ J

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Effects of relaxin and estrogens on bone remodeling markers, receptor activator of NF-kB ligand (RANKL) and osteoprotegerin (OPG), in rat adjuvant-induced arthritis

Cited by 45 publications

References 41 publications

Adjunctive Antimicrobial Photodynamic Treatment of Experimentally Induced Periodontitis in Rats With Ovariectomy

Adjunctive Antimicrobial Photodynamic Treatment of Experimentally Induced Periodontitis in Rats With Ovariectomy

(5R)-5-hydroxytriptolide (LLDT-8) prevents collagen-induced arthritis through OPG/RANK/RANKL signaling in a rat model of rheumatoid arthritis

Dysregulated Atrial Gene Expression of Osteoprotegerin/Receptor Activator of Nuclear Factor-.KAPPA.B (RANK)/RANK Ligand Axis in the Development and Progression of Atrial Fibrillation

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