IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes

Watanabe, Yusuke; Namba, Aki; Aida, Yasuhiro; Honda, Kazuo; Tanaka, Hideki; Suzuki, Naoto; Matsumura, Hideo; Maeno, Masao

doi:10.1155/2009/308596

Cited by 14 publications

(16 citation statements)

References 37 publications

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“…It has also been shown that IL-1β suppresses osteoclast formation by increasing osteoprotegerin 13) , and these phenomena result in increased prostaglandin E 2 production 14) .…”

Section: Introductionmentioning

confidence: 99%

Influence of Compressive Force and IL-1^|^beta; on Metabolism of the Extracellular Matrix in Human Chondrocytes

Nakayama

Aida

Watanabe

et al. 2012

J. Hard Tissue Biology.

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“…It has also been shown that IL-1β suppresses osteoclast formation by increasing osteoprotegerin 13) , and these phenomena result in increased prostaglandin E 2 production 14) .…”

Section: Introductionmentioning

confidence: 99%

Influence of Compressive Force and IL-1^|^beta; on Metabolism of the Extracellular Matrix in Human Chondrocytes

Nakayama

Aida

Watanabe

et al. 2012

J. Hard Tissue Biology.

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“…Recently, Namba et al (22) reported that IL-6 and sIL-6r suppress differentiation of chondrocytes and induce expression of cartilage matrix proteins. On the other hand, Watanabe et al (15) reported that IL-1β suppressed the formation of osteoclasts by increasing OPG production via an autocrine mechanism involving the production of celecoxib-related prostaglandins, primarily PGE 2 , by chondrocytes. Thus, the present study focused on osteoclastic differentiation mediated by RANK/RANKL/OPG, through which chondrocytes communicate with osteoclast precursors.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, IL-6 is closely associated (9)(10)(11)(12). RANKL is highly expressed on osteoblasts/stroma cells and on the primitive mesenchymal cells surrounding the cartilaginous anlagen, ie, proliferating and hypertrophying chondrocytes (13)(14)(15). Osteoclast precursors recognize RANKL via RANK expressed on their cell surfaces and differentiate into mononuclear perfusion osteoclasts (POCs) in the presence of M-CSF.…”

Section: Introductionmentioning

confidence: 99%

“…Consequently, OPG is an effective inhibitor of osteoclast maturation and activation (9,14,16). Recently, Watanabe et al (15) reported that RANKL, M-CSF, and OPG were expressed in chondrocytes derived from normal human femoral cartilage. PGE 2 has been detected in TMJ synovial fluid from patients with internal derangement of the joint (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

“…In a previous study that examined the effects of cytokines on osteoclastic differentiation, Watanabe et al (15) demonstrated that IL-1β suppressed the formation of osteoclast-like cells by increasing OPG production and decreasing M-CSF production in chondrocytes. Their data suggested that OPG induction may be achieved through an autocrine mechanism involving celecoxib-related prostaglandins, primarily PGE 2 .…”

Section: Introductionmentioning

confidence: 99%

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Interleukin-6 and soluble interleukin-6 receptor suppress osteoclastic differentiation by inducing PGE2 production in chondrocytes

Honda¹

2011

J Oral Sci

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This study examined how interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6r) influence osteoclastic differentiation through the function of chondrocytes. Chondrocytes were cultured with or without IL-6 and/or sIL-6r in the presence or absence of NS398, a specific inhibitor of cyclooxygenase (COX)-2, for up to 28 days. Chondrocytes were also cultured with or without IL-6 and sIL-6r for 28 days, and the conditioned medium from cells cultured without IL-6 and sIL-6r was used to induce differentiation of RAW264.7 cells into osteoclast precursors. Osteoclastic differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining. Expression of osteoprotegerin (OPG), receptor activator of NF-κB ligand (RANKL), COX-2, and prostaglandin E 2 (PGE 2 ) increased in cells exposed to IL-6 and sIL-6r, whereas expression of macrophage colony-stimulating factor (M-CSF) and bone resorption-related enzymes decreased. NS398 blocked the stimulatory/suppressive effects of IL-6 and sIL-6r on the expression of OPG, RANKL, and M-CSF. Fewer TRAP-positive multinucleated cells were detected after treatment with conditioned medium from IL-6-and sIL-6r-treated chondrocytes than after treatment with conditioned medium from untreated chondrocytes. These results suggest that IL-6 and sIL6r interfere with osteoclast function through the involvement of chondrocytes. Specifically, they appear to suppress the differentiation of osteoclast precursors into osteoclasts by inducing chondrocytic PGE 2 production, which, in turn, increases OPG secretion and decreases M-CSF secretion by chondrocytes. (J Oral Sci 53, 87-96, 2011)

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Modulatory effects of silibinin in cell behavior during osteogenic phenotype

Fernandes

Veiga

Peraçoli

et al. 2019

J of Cellular Biochemistry

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Natural molecules, such as flavonoid, are very welcome strategies to modulate bone turnover. This prompted us to comprehend better the effect of silibinin on osteoblast metabolism, mainly considering intracellular pathways able to drive cell adhesion to differentiation. By exploring in vitro approaches, our data show a modulatory effect of the silibinin (200 μg/mL) on the osteoblast intracellular signaling, contributing with decisive pathways governing cell adhesion, differentiation, and further mineralization, recapitulating important stages of osteogenesis. Within the first 24 hours of adhesion (acute stage), osteoblasts respond to silibinin by rearranging their cytoskeleton and start mechanisms responsible to extracellular matrix (ECM) remodeling, which reach intense profile at 28 days of treatment (chronic stage) by favoring matrix metalloproteinases (MMPs-2, and -9) activities, concomitant to mineralizing phenotype. Importantly, silibinin seems to reprogram genes related to inflammatory landscape and significantly upmodulating osteoprotegerin (>25 foldchanges), signaling molecule involved with osteoclastogenesis. Altogether, our results show for the first time that silibinin drives in vitro osteoblast differentiation by requiring specific intracellular signaling. In conju nction, this molecular landscape contributes to understand the effect of silibinin on osteoblasts performance and open novel therapeutic possibilities to silibinin in bone disorders, such as osteoporosis. K E Y W O R D S bone, flavonoid, inflammation, osteoblast, remodeling, silibinin

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IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes

Cited by 14 publications

References 37 publications

Influence of Compressive Force and IL-1^|^beta; on Metabolism of the Extracellular Matrix in Human Chondrocytes

Influence of Compressive Force and IL-1^|^beta; on Metabolism of the Extracellular Matrix in Human Chondrocytes

Interleukin-6 and soluble interleukin-6 receptor suppress osteoclastic differentiation by inducing PGE2 production in chondrocytes

Modulatory effects of silibinin in cell behavior during osteogenic phenotype

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