The CCL2/CCR2 Axis Enhances Vascular Cell Adhesion Molecule-1 Expression in Human Synovial Fibroblasts

Lin, Yu‐Min; Hsu, Chin‐Jung; Liao, Yuan-Ya; Chou, Ming-Chih; Tang, Chih‐Hsin

doi:10.1371/journal.pone.0049999

Cited by 35 publications

(36 citation statements)

References 38 publications

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“…Besides, recent studies have demonstrated that CCL2 increases vascular cell adhesion molecule 1 (VCAM-1) expression in human OA synovial fibroblasts via a cascade of signalling pathways, and CCL2-induced VCAM-1 expression promoted monocyte adhesion to human OA synovial fibroblasts. 16 These data suggest that CCL2 may play crucial roles during OA pathogenesis and progression or may even be important in OA symptomatology. However, there have been no studies illustrating the relationship between serum and SF concentrations of CCL2 and the symptomatic severity of OA.…”

Section: Introductionmentioning

confidence: 82%

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Jiang

2014

Ann Clin Biochem

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Objective: Serum and synovial fluid (SF) chemokine ligand 2 (CCL2)/monocyte chemoattractant protein 1 (MCP-1) concentrations have been identified to be increased in osteoarthritis (OA) patients. The scope of this study was to examine CCL2 concentrations in serum and SF of knee OA patients and to explore their association with patientreported symptomatic severity. Method: One hundred and sixty-one knee OA patients and 138 healthy controls were enrolled into the study from our hospital. We collected Western Ontario and McMaster Universities Arthritis Index (WOMAC) scores from OA patients and measured CCL2 concentrations in serum and SF using enzyme-linked immunosorbent assay method, and correlation between WOMAC scores and CCL2 concentrations were analysed. Results: CCL2 concentrations in SF instead of serum were independently and positively associated with self-reported greater pain (r ¼ 0.460, P < 0.001) and physical disability (r ¼ 0.561, P < 0.001) in OA patients. Conclusion: CCL2 in SF might serve as a novel and reliable biomarker for assessing symptomatic severity of OA.

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Section: Introductionmentioning

confidence: 82%

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Jiang

2014

Ann Clin Biochem

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“…MSCs are known to release microvesicles containing proteins, lipids, mRNA, and microRNAs; microvesicles transfer the adhesion molecule CD41 from platelets to endothelial cells42, implying that MSCs might be able to release VCAM-1 mRNA-containing microvesicles that might induce VCAM-1 expression on T cells. CCL2 is also known to induce VCAM-1 expression on synovial fibroblasts43, implying that CCL2 produced by MSCs might increase VCAM-1 expression on T cells. Our future data will help to reveal how MSCs inhibit T cells in a CCL2-dependent contact-inhibition manner.…”

Section: Discussionmentioning

confidence: 99%

CCL2 deficient mesenchymal stem cells fail to establish long-lasting contact with T cells and no longer ameliorate lupus symptoms

Lee

Kim

et al. 2017

Sci Rep

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Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease characterized by autoantibody production. Mesenchymal stem cells (MSCs) ameliorate SLE symptoms by targeting T cells, whereas the mechanisms of their efficacy remain incompletely understood. In this study, we show that transfer of human MSCs increased MRL.Faslpr mouse survival, decreased T cell infiltration in the kidneys, and reduced T cell cytokine expression. In vitro, allogeneic mouse MSCs inhibited MRL.Faslpr T cell proliferation and cytokine production. Time-lapse imaging revealed that MSCs recruited MRL.Faslpr T cells establishing long-lasting cellular contacts by enhancing T cell VCAM-1 expression in a CCL2-dependent manner. In contrast, CCL2 deficient MSCs did not induce T cell migration and VCAM-1 expression, resulting in insufficient cell-cell contact. Consequently, CCL2 deficient MSCs did not inhibit IFN-γ production by T cells and upon transfer no longer prolonged survival of MRL.Faslpr mice. Taken together, our imaging study demonstrates that CCL2 enables the prolonged MSC–T cell interactions needed for sufficient suppression of autoreactive T cells and helps to understand how MSCs ameliorate symptoms in lupus-prone MRL.Faslpr mice.

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“…51 Another group demonstrated FLS upregulate Vascular Cell Adhesion Molecule-1 (VCAM-1) in response to CCL2 to promote monocyte adhesion in culture. 52 Still others have demonstrated a role for CCL5/CCR5 signaling in promoting FLS IL-6 production. 53 Although these studies are interesting and suggest mechanisms by which chemokines promote inflammatory and catabolic activity of synoviocytes, additional investigation is needed to understand which chemotactic factors perpetuate synovitis and modulate the activity of the synovial tissue in vivo.…”

Section: Chemokines and Synovial Inflammationmentioning

confidence: 99%

Chemokines and inflammation in osteoarthritis: Insights from patients and animal models

Scanzello

2017

Journal Orthopaedic Research

172

140

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Evidence has been building that the pathologic drive for development of osteoarthritis (OA) involves more than simple mechanical “wear and tear.” Inflammatory mechanisms play an important role in the tissue response to joint injury, and are involved in development of post-traumatic OA. Inflammation also appears integral to the progression of OA, whether post-traumatic or spontaneous, contributing to the evolution of joint tissue degradation and remodeling as well as joint pain. Both patient-based studies and in vivo models of disease have shed light on a number of inflammatory pathways and mediators that impact various aspects of this disease, both structurally and symptomatically. Recent work in this field has implicated inflammatory chemokines in osteoarthritis pathogenesis. Expression of multiple chemokines and their receptors is modulated during disease in both patients and animal models. Although best known for their effects on leukocyte migration and trafficking within the immune system, chemokines can have a wide variety of effects on both motile and non-motile cell types, impacting proliferation, differentiation, and activation of cellular responses. Their role in OA models has also demonstrated diverse effects on disease that exemplify their wide-ranging effects. Understanding how these important mediators of inflammation impact joint disease, and whether they can be targeted therapeutically, is actively being investigated by many groups in this field. This narrative review focuses on evidence published within the last 5 years highlighting chemokine-mediated pathways with mechanistic involvement in osteoarthritis and joint tissue repair.

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The CCL2/CCR2 Axis Enhances Vascular Cell Adhesion Molecule-1 Expression in Human Synovial Fibroblasts

Cited by 35 publications

References 38 publications

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

CCL2 deficient mesenchymal stem cells fail to establish long-lasting contact with T cells and no longer ameliorate lupus symptoms

Chemokines and inflammation in osteoarthritis: Insights from patients and animal models

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