Osteopontin as a positive regulator in the osteoclastogenesis of arthritis

Ishii, Taeko; Ohshima, Shiro; Ishida, Tomohiro; Mima, Toru; Tabunoki, Youichiro; Kobayashi, Hideyuki; Maeda, Masahiro; Uede, Toshimitsu; Liaw, Lucy; Kinoshita, Naokazu; Kawase, Ichiro; Saeki, Yukihiko

doi:10.1016/j.bbrc.2004.02.124

Cited by 43 publications

(36 citation statements)

References 32 publications

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“…In contrast, a 3.5-fold increase in adherent cells was observed in OPN treated Nf1ϩ/Ϫ cultures compared with PBS treated Nf1ϩ/Ϫ OCLs. OPN has been known to regulate OCL motility (22), and we further examined OPNmediated OCL migration using the transwell assay. Nf1ϩ/Ϫ OCLs demonstrated significantly higher OCL migration when compared with WT cells under basal unstimulated condition.…”

Section: Resultsmentioning

confidence: 99%

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Ras Dependent Paracrine Secretion of Osteopontin by Nf1+/− Osteoblasts Promote Osteoclast Activation in a Neurofibromatosis Type I Murine Model

Liu

Zhang

et al. 2009

Pediatr Res

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Neurofibromatosis type 1 (NF1) is a pandemic genetic disorder characterized by malignant and nonmalignant manifestations, including skeletal abnormalities, such as osteoporosis, scoliosis, short stature, and pseudarthrosis. Recent studies in genetically inbred mice and from human patients with NF1 have identified multiple gains in osteoclast (OCL) functions both in vitro and in vivo. Given that osteoblasts secrete cytokines that promote OCL maturation/activation, we sought to identify whether haploinsufficiency of Nf1 (Nf1ϩ/Ϫ) osteoblasts and their precursors secrete cytokines that have a central role in this process. Osteoblast conditioned media (OBCM) from Nf1ϩ/Ϫ osteoblasts promoted OCL migration and bone resorption compared with WT OBCM. Osteopontin (OPN), a matrix protein found in mineralized tissues and pivotal in modulating OCL functions, was present in increased concentrations in Nf1ϩ/Ϫ osteoblasts. Addition of OPN neutralizing antibody to Nf1ϩ/Ϫ OBCM diminished the gain in bioactivity on OCL functions, including OCL migration and bone resorption. Our study identifies an important paracrine loop whereby elevated secretion of OPN by osteoblasts activate Nf1ϩ/Ϫ OCLs that already have an intrinsic propensity for bone resorption leading to osteopenia and osteoporosis. (Pediatr Res 65: 613-618, 2009)

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Section: Resultsmentioning

confidence: 99%

“…It also has been known that OPN is a positive regulator for osteoclastogenesis (22). El-Tanani et al (26) reported an association of Ras with OPN expression in malignant cells.…”

Section: Discussionmentioning

confidence: 99%

Ras Dependent Paracrine Secretion of Osteopontin by Nf1+/− Osteoblasts Promote Osteoclast Activation in a Neurofibromatosis Type I Murine Model

Liu

Zhang

et al. 2009

Pediatr Res

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“…It is also implicated in tissue remodeling and destruction in several diseases such as atherosclerosis and granulomatous inflammation (22,51). In RA it is mainly expressed in synovial tissues of patients, predominantly in the lining layer (31,52). Interestingly, SPP1 protein levels in plasma show no significant differences between RA and OA Fig.…”

Section: Discussionmentioning

confidence: 99%

Molecular signatures and new candidates to target the pathogenesis of rheumatoid arthritis

Ungethuem

Haeupl

Witt

et al. 2010

Physiological Genomics

117

103

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“…OPN Ϫ/Ϫ mice have also been reported to have attenuated host resistance against Mycobacterium bovis bacillus Calmette-Guérin (2) but, unexpectedly, normal host defense against Borrelia burgdorferi and the concurrent development of arthritis (3). Murine deficiency in OPN has been demonstrated to ameliorate the development of several autoimmune diseases including experimental autoimmune encephalomyelitis (EAE) (4,5), anti-type II collagen Ab-induced arthritis (CAIA) (6), and collagen-induced arthritis (CIA) (7), although contradictory reports have been published (8,9). We have investigated the role of OPN in experimental autoimmune myocarditis, a CD4 ϩ T cell-mediated autoimmune model, and demonstrated that OPN is not required for the development of the disease (our manuscript in preparation).…”

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confidence: 99%

Osteopontin Is Not Required for the Development of Th1 Responses and Viral Immunity

Abel

Freigang²,

Bachmann³

et al. 2005

The Journal of Immunology

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Osteopontin (OPN) has been defined as a key cytokine promoting the release of IL-12 and hence inducing the development of protective cell-mediated immunity to viruses and intracellular pathogens. To further characterize the role of OPN in antiviral immunity, OPN-deficient (OPN−/−) mice were analyzed after infection with influenza virus and vaccinia virus. Surprisingly, we found that viral clearance, lung inflammation, and recruitment of effector T cells to the lung were unaffected in OPN−/− mice after influenza infection. Furthermore, effector status of T cells was normal as demonstrated by normal IFN-γ production and CTL lytic activity. Moreover, activation and Th1 differentiation of naive TCR transgenic CD4+ T cells by dendritic cells and cognate Ag was normal in the absence of OPN in vitro. Contrary to a previous report, we found that OPN−/− mice mounted a normal immune response to Listeria monocytogenes. In conclusion, OPN is dispensable for antiviral immune responses against influenza virus and vaccinia virus.

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Osteopontin as a positive regulator in the osteoclastogenesis of arthritis

Cited by 43 publications

References 32 publications

Ras Dependent Paracrine Secretion of Osteopontin by Nf1+/− Osteoblasts Promote Osteoclast Activation in a Neurofibromatosis Type I Murine Model

Ras Dependent Paracrine Secretion of Osteopontin by Nf1+/− Osteoblasts Promote Osteoclast Activation in a Neurofibromatosis Type I Murine Model

Molecular signatures and new candidates to target the pathogenesis of rheumatoid arthritis

Osteopontin Is Not Required for the Development of Th1 Responses and Viral Immunity

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