Synovial expression of osteopontin correlates with angiogenesis in juvenile idiopathic arthritis

Gattorno, Marco; Gregorio, Andrea; Ferlito, Francesca; Gerloni, Valeria; Parafioriti, Antonina; Felici, Enrico; Sala, Elena Marzia; Gambini, Claudio; Picco, Paolo; Martini, Alberto

doi:10.1093/rheumatology/keh250

Cited by 31 publications

(31 citation statements)

References 43 publications

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“…We report here that OPN expression in adipose tissue increases with obesity and that plasma levels increase during the development of DIO OPN, suggesting a potential novel function of OPN for obesity-associated inflammatory and metabolic changes in adipose tissue. OPN plasma levels are elevated in various inflammatory diseases, including atherosclerosis (26), inflammatory bowel disease (27), granulomatous inflammatory diseases (28), rheumatoid arthritis (29), and mul-…”

Section: Discussionmentioning

confidence: 99%

Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

Nomiyama

Pérez-Tilve

Ogawa³

et al. 2007

J. Clin. Invest.

344

324

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Obesity is associated with a state of chronic, low-grade inflammation characterized by abnormal cytokine production and macrophage infiltration into adipose tissue, which may contribute to the development of insulin resistance. During immune responses, tissue infiltration by macrophages is dependent on the expression of osteopontin, an extracellular matrix protein and proinflammatory cytokine that promotes monocyte chemotaxis and cell motility. In the present study, we used a murine model of diet-induced obesity to examine the role of osteopontin in the accumulation of adipose tissue macrophages and the development of insulin resistance during obesity. Mice exposed to a high-fat diet exhibited increased plasma osteopontin levels, with elevated expression in macrophages recruited into adipose tissue. Obese mice lacking osteopontin displayed improved insulin sensitivity in the absence of an effect on diet-induced obesity, body composition, or energy expenditure. These mice further demonstrated decreased macrophage infiltration into adipose tissue, which may reflect both impaired macrophage motility and attenuated monocyte recruitment by stromal vascular cells. Finally, obese osteopontin-deficient mice exhibited decreased markers of inflammation, both in adipose tissue and systemically. Taken together, these results suggest that osteopontin may play a key role in linking obesity to the development of insulin resistance by promoting inflammation and the accumulation of macrophages in adipose tissue.

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Section: Discussionmentioning

confidence: 99%

Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

Nomiyama

Pérez-Tilve

Ogawa³

et al. 2007

J. Clin. Invest.

344

324

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“…It also promotes angiogenesis and inhibits immune reaction, which induces the invasion and metastasis of tumor cells (23). OPN is highly expressed in the articular cartilage, synovial fluid and synovium of osteoarthritis patients, while its expression has been positively correlated to the severity of the disease, indicating that OPN is closely associated with the development and progression of osteoarthritis (24,25). In animal experiments, it was observed that OPN gene-deficient mice had a strong ability to resist collagen-induced arthritis (26).…”

Section: Discussionmentioning

confidence: 99%

Roles of microRNA-539 and osteopontin in rheumatoid arthritis

Liu

Qian

et al. 2017

Exp Ther Med

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Abstract. The present study aimed to investigate the role and mechanism of microRNA-539 (miR-539) in rheumatoid arthritis (RA). A total of 68 RA patients and 46 osteoarthritis patients were enrolled into the current study. Peripheral blood and joint fluid were collected prior to treatment. Reverse transcription-quantitative polymerase chain reaction was performed to detect osteopontin (OPN) mRNA and miR-539 expression levels, while ELISA and western blot analysis were applied to detect OPN protein expression. In addition, bioinformatics analysis predicted that miR-539 directly targeted OPN, while dual-luciferase assay was used to validate this finding. Furthermore, agomiR-539 transfection and OPN knockdown by siRNA were conducted in MH7A cells, and MTT assay was used to detect MH7A cell proliferation. The results indicated that OPN was significantly increased in the blood and joint fluid of RA patients, while miR-539 expression was significantly decreased in the two types of specimens (P<0.05). Subsequent to silencing OPN by siRNA, the proliferation of MH7A cells was decreased (P<0.05). Following upregulation of miR-539, OPN expression was significantly decreased and cell proliferation was inhibited. Dual-luciferase assay revealed that miR-539 regulated OPN expression through complementary binding to 3'-untranslated region. OPN was also significantly increased in the blood and joint fluid of RA patients, which may be associated with the downregulation of miR-539. Thus, miR-539 may promote the development and progression of RA through regulating OPN. IntroductionRheumatoid arthritis (RA) is a systemic autoimmune disease characterized by symmetrical arthritis, which may invade the heart, lung, kidney, artery, nerve and eyes (1,2). The prevalence rate of RA ranks first among autoimmunity connective tissue diseases (3). The average incidence of RA is 0.5-1% worldwide, while it is 0.32-0.36% in China (4). RA can occur at any age with a high incidence rate, and the common age of incidence is 40-60 years. The majority of the RA patients are women, and the incidence rate is 2-3 times higher in comparison with that in men (5).It has been reported that numerous microRNAs (miRs) participate in the development and progression of RA (6-8).In addition, miR-539 has been observed to be significantly upregulated in patients with heart failure (9), in the blood of patients with alcoholic hepatitis (10), and in human osteosarcoma cells (11). All these findings indicated that miR-539 is closely associated with the disease development. However, the role of miR-539 in RA remains unclear.Osteopontin (OPN), also known as secreted phosphoprotein 1 or early T-lymphocyte activation 1, is a potential promoter among inflammatory cytokines (12). A large numbers of OPN surface receptors are expressed in synovial cells, which combined with OPN to induce signaling transduction and influence the adhesion and proliferation of synovial cells (13). In RA and juvenile idiopathic arthritis patients, OPN protein has been reported to be significantly i...

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“…Both OPN and VEGF have significantly elevated expression in the synovial fluid of patients with juvenile idiopathic arthritis. The secretion of OPN correlates positively with VEGF concentration as well as vascularization of the inflamed synovial tissue [61]. VEGF and OPN co-expression is associated with angiogenesis and unfavorable outcome in various cancers.…”

Section: Co-expression Of Opn and Vegfmentioning

confidence: 97%

“…Higher levels Treatment for vascular diseases [158] Angiogenesis Heart Higher levels Valvular calcification, rheumatic heart disease [33] Angiogenesis Blood vessels Endothelial cells Distinct pathways [74] Angiogenesis Blood vessels Endothelial cells OPN in angiogenesis [75] Angiogenesis Blood vessels Endothelial cells OPN in angiogenesis [198] Angiogenesis, bone regeneration Bone Murine preosteoblastic cells Higher levels Incorporation of bioactive inorganic particles [39] Angiogenesis, bone-mineral metabolic disorders Bone/kidney Distinct pathways Matrix extracellular phosphoglycoprotein overexpression [28] Angiogenesis, cancer Brain VEGF induces OPN Glioblastoma, malignant [29] Angiogenesis, cancer Brain VEGF induces OPN Glioblastoma, malignant [37] Angiogenesis, cancer Blood vessels Endothelial progenitor cells, human glioma cells Distinct pathways Glioma [11] Angiogenesis, cancer Breast Breast adenocarcinoma cells OPN induces VEGF [46] Angiogenesis, cell motility Kidney Kidney endothelial and epithelial cells Distinct expression Bim deficiency [61] Angiogenesis, inflammation Joint Higher levels Arthritis, juvenile idiopathic [104] Angiogenesis Bone regeneration Bone Mesenchymal stem cells Higher levels Allogeneic mesenchymal stem cell transplantation [197] Bone regeneration Bone Osteoblasts Higher levels Low intensity pulsed ultrasound [164] Bone regeneration Bone Higher levels Marrow ablation, femoral [209] Bone regeneration Mouth Periodontal ligament and Endothelial cells Upregulated Periodontal tissue, effect of BDNF [169] Bone regeneration Bone Murine preosteoblastic cells Higher levels Thermal stress conditioning and growth factors [1] Bone regeneration Bone Circulating marrow-derived osteoblast progenitor cells Co-expression [165] Bone remodeling Bone Higher levels Stress fracture healing [163] Bone repair Bone Higher levels Fractures, long bone [25] Bone repair Bone Bone marrow stromal cells VEGF induces OPN [193] Bone repair Bone Higher levels Distraction osteogenesis [194] Bone repair Bone Primary human osteoblast cells Higher levels Distraction osteogenesis [195] Bone repair Bone Higher levels Distraction osteogenesis, mandibular [203] Bone repair, angiogenesis Bone Higher levels Fractures, treatment with formononetin …”

Section: Induction Of Opn By Vegfmentioning

confidence: 99%

Interactions between osteopontin and vascular endothelial growth factor: Implications for cancer

Ramchandani

Weber

2015

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Synovial expression of osteopontin correlates with angiogenesis in juvenile idiopathic arthritis

Cited by 31 publications

References 43 publications

Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice

Roles of microRNA-539 and osteopontin in rheumatoid arthritis

Interactions between osteopontin and vascular endothelial growth factor: Implications for cancer

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