Cross-Communication Between Knee Osteoarthritis and Fibrosis: Molecular Pathways and Key Molecules

Bolia, Ioanna K; Mertz, Kevin; Faye, Ethan; Sheppard, J.A.; Telang, Sagar; Bogdanov, Jacob; Hasan, Laith K; Haratian, Aryan; Evseenko, Denis; Weber, Alexander E.; Petrigliano, Frank A.

doi:10.2147/oajsm.s321139

Cited by 5 publications

(6 citation statements)

References 98 publications

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“…ACAN mRNA expression showed downregulation in OA sf-MSCs compared with H cells, supported by DMMB assay, specific for GAG quantification, which enforces the reduced chondrogenic potential of OA sf-MSCs. Supposing to observe a reduced synthesis of the chondrogenic markers in OA sf-MSCs, we speculate that the unexpected expression of COL2A1 marker, such as H sf-MSCs, could be related to a fibrotic condition which typically occurs in the articular joint during OA progression and plays a critical role in OA pathogenesis as well as cartilage destruction [ 55 , 56 ]. The reduced synthesis of GAG supports this hypothesis, but further investigations, based on a higher number of donors, are needed to confirm the assumption.…”

Section: Discussionmentioning

confidence: 99%

Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells

Teti

Mazzotti

Gatta

et al. 2023

IJMS

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Osteoarthritis (OA) is described as a chronic degenerative disease characterized by the loss of articular cartilage. Senescence is a natural cellular response to stressors. Beneficial in certain conditions, the accumulation of senescent cells has been implicated in the pathophysiology of many diseases associated with aging. Recently, it has been demonstrated that mesenchymal stem/stromal cells isolated from OA patients contain many senescent cells that inhibit cartilage regeneration. However, the link between cellular senescence in MSCs and OA progression is still debated. In this study, we aim to characterize and compare synovial fluid MSCs (sf-MSCs), isolated from OA joints, with healthy sf-MSCs, investigating the senescence hallmarks and how this state could affect cartilage repair. Sf-MSCs were isolated from tibiotarsal joints of healthy and diseased horses with an established diagnosis of OA with an age ranging from 8 to 14 years. Cells were cultured in vitro and characterized for cell proliferation assay, cell cycle analysis, ROS detection assay, ultrastructure analysis, and the expression of senescent markers. To evaluate the influence of senescence on chondrogenic differentiation, OA sf-MSCs were stimulated in vitro for up to 21 days with chondrogenic factors, and the expression of chondrogenic markers was compared with healthy sf-MSCs. Our findings demonstrated the presence of senescent sf-MSCs in OA joints with impaired chondrogenic differentiation abilities, which could have a potential influence on OA progression.

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Section: Discussionmentioning

confidence: 99%

Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells

Teti

Mazzotti

Gatta

et al. 2023

IJMS

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“…Google Scholar was also used as a complementary search engine. A manual search of the reference lists of past reviews was performed 140 . Furthermore, citation searching was performed on the original records using Web of Science as recommended 125 .…”

Section: Star Methodsmentioning

confidence: 99%

Network-based cytokine inference implicates Oncostatin M as a driver for inflammation phenotype of knee osteoarthritis

Iijima

Zhang

Ambrosio

et al. 2023

Preprint

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Inflammatory cytokines released by the synovium after trauma disturb the gene regulatory network and have been implicated in the pathophysiology of osteoarthritis. A mechanistic understanding of how aging perturbs this process can help identify novel interventions. Here, we introduced network paradigms to simulate cytokine-mediated pathological communication between the synovium and cartilage. Cartilage functional network analysis of injured young and aged murine knees revealed aberrant matrix remodeling as a transcriptomic response unique to aged knees. This finding was concomitant with accelerated cartilage degradation, as identified through meta-analysis of histological assessments. Next, cytokine inference with network propagation on the cartilage network uncovered IL6 family member, Oncostatin M (OSM), as a driver for osteoarthritis. Pharmacological manipulations confirmed that the aberrant matrix remodeling is attributed, at least partly, to downstream signals of OSM, but not IL6. These analyses implicate OSM as a promising therapeutic target to ameliorate osteoarthritis in aging through improved synovium-cartilage communication.

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“…[ 21 ] Synovial fibrosis exists in different stages of OA, is stimulated by synovitis. For example, IL‐1β is not only a key regulator of TGF‐β, but also stimulates IL‐1β receptors on fibroblasts, leading to fibroblast proliferation and promoting fibrosis, [ 119 ] and IL‐6 promotes fibrosis by activating the Notch/STAT3 pathway. [ 120 ] Recent studies have found that synovial fibroblast and macrophage pyroptosis is involved in synovial fibrosis and is associated with the release of inflammatory factors (IL‐1β, IL‐18) due to activated NLRP3 inflammasome.…”

Section: The Pathological Change Of Synovial Cells In Oamentioning

confidence: 99%

The potential role of synovial cells in the progression and treatment of osteoarthritis

Zou

Han

Yang³

et al. 2023

Exploration

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Osteoarthritis (OA), the commonest arthritis, is characterized by the progressive destruction of cartilage, leading to disability. The Current early clinical treatment strategy for OA often centers on anti‐inflammatory or analgesia medication, weight loss, improved muscular function and articular cartilage repair. Although these treatments can relieve symptoms, OA tends to be progressive, and most patients require arthroplasty at the terminal stages of OA. Recent studies have shown a close correlation between joint pain, inflammation, cartilage destruction and synovial cells. Consequently, understanding the potential mechanisms associated with the action of synovial cells in OA could be beneficial for the clinical management of OA. Therefore, this review comprehensively describes the biological functions of synovial cells, the synovium, together with the pathological changes of synovial cells in OA, and the interaction between the cartilage and synovium, which is lacking in the present literature. Additionally, therapeutic approaches based on synovial cells for OA treatment are further discussed from a clinical perspective, highlighting a new direction in the treatment of OA.

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Cross-Communication Between Knee Osteoarthritis and Fibrosis: Molecular Pathways and Key Molecules

Cited by 5 publications

References 98 publications

Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells

Implication of Cellular Senescence in Osteoarthritis: A Study on Equine Synovial Fluid Mesenchymal Stromal Cells

Network-based cytokine inference implicates Oncostatin M as a driver for inflammation phenotype of knee osteoarthritis

The potential role of synovial cells in the progression and treatment of osteoarthritis

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