Osteoprotegerin: Multiple partners for multiple functions

Baud’huin, Marc; Duplomb, Laurence; Téletchéa, Stéphane; Lamoureux, François; Ruiz-Velasco, Carmen; Maillasson, Mike; Rédini, Françoise; Heymann, Marie-Françoise; Heymann, Dominique

doi:10.1016/j.cytogfr.2013.06.001

Cited by 124 publications

(119 citation statements)

References 81 publications

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“…RANK/RANKL interactions, which are essential for the survival, differentiation, and activation of osteoclasts, can be modulated by OPG, a decoy receptor for RANKL. However, the effects of OPG are complex, as it has multiple binding partners; in addition to RANKL, it also interacts with TNF-related apoptosis-inducing ligand (TRAIL) (Baud'huin et al 2013). TRAIL induces apoptosis in numerous tumor cell lines, and OPG is able to block TRAIL-induced apoptosis (Emery et al 1998;Neville-Webbe et al 2004;Shipman and Croucher 2003).…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, OPG treatment strongly increases the number of adherent human CD14 ? monocytes, with an activation of the Akt/PI3-kinase signaling pathway in these cells (Baud'huin et al 2013) and induces leukocyte adhesion to endothelial cells within 15 min (Zauli et al 2007). These reports, in combination with our findings that exposure of preosteoclasts to OPG stimulates integrin b3 expression and actin ring formation at the cell periphery and also strongly enhances the growth of osteoclast precursors within 24 h of exposure, suggests that OPG enhances adhesion by modulating the expression of the proteins within podosomes and inhibits preosteoclast apoptosis by binding to TRAIL.…”

Section: Discussionmentioning

confidence: 99%

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Osteoprotegerin exposure at different stages of osteoclastogenesis differentially affects osteoclast formation and function

Zhao

Dai

et al. 2015

Cytotechnology

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This study aimed to investigate the effects of osteoprotegerin (OPG), a decoy receptor for receptor activator for nuclear factor jB ligand (RANKL), during the various stages of osteoclast differentiation, and additionally investigate its effects on osteoclast adhesion and activity. RAW264.7 murine monocytic cells were incubated with macrophage colony-stimulating factor and RANKL for 1, 3, 5, or 7 days, followed by an additional 24-h incubation in the presence or absence of OPG (80 ng/mL). We examined osteoclast differentiation and adhesion capacity using the tartrate-resistant acid phosphatase (TRAP) assay and immunofluorescence microscopy, and additionally examined cell growth in real time using the xCELLigence system. Furthermore, the expression levels of TRAP, RANK, integrin b3, matrix metalloproteinase 9, cathepsin K, carbonic anhydrase II, and vesicular-type H ? -ATPase A1 were examined using western blotting. OPG exposure on day 1 enhanced the osteoclast growth curve as well as adhesion, and increased RANK and integrin b3 expression. In contrast, exposure to OPG at later time points (days 3-7) inhibited osteoclast differentiation, adhesion structure formation, and protease expression. In conclusion, the biological effects of OPG exposure at the various stages of osteoclast differentiation were varied, and included the enhanced adhesion and survival of preosteoclasts, the block of differentiation from the early to the terminal stages of osteoclastogenesis, and suppression of mature osteoclast activation following OPG exposure during the terminal differentiation stage, suggesting that the effects of OPG exposure differ based on the stage of differentiation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Osteoprotegerin exposure at different stages of osteoclastogenesis differentially affects osteoclast formation and function

Zhao

Dai

et al. 2015

Cytotechnology

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“…It prevents the proliferation and differentiation of osteoclasts that increases bone density and volume [9]. The evidence showing the importance of OPG in bone biology was provided by studies based on genetic experiments [10][11][12].…”

Section: Int Conf Society Health Welfare 2014mentioning

confidence: 99%

Osteopontin, osteocalcin, and osteoprotegerin expression in human tissue affected by cleft lip and palate

Smane

Pilmane

2016

SHS Web Conf.

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Abstract. Cleft lip and palate (CLP) is a common congenital anomaly with a complex etiology which has not been elucidated yet. This study investigated whether expression of osteopontin (OPN), osteoprotegerin (OPG), and osteocalcin (OC), which are essential for the normal craniofacial bone remodelling, is not regulated in children with CLP. Alveolar bone tissue samples were obtained from patients with complete bilateral (CB) CLP (n = 14) during corrective plastic surgery and unaffected control subjects (n = 9). OPN, OPG, and OC expression was assessed by immunohistochemistry, and data were analyzed with the Mann-Whitney test. OPN expression was observed only sporadically in the alveolar bone of 3 patients, in contrast to the control group (z = − 2.962; P < 0.003). The number of OPG-positive bone cells varied from occasional to moderate, in contrast to the control group (z = − 2.247; P = 0.025). OC-positive osteocytes were present in moderate to numerous numbers in both patients and controls, with no significant difference between them (z = − 1.356; P < 0.175). The prominent expression of OC characteristic for CBCLP affected hard tissue indicates a high potential of bone mineralization. Few OPG-positive osteocytes in the bone tissue implicate the disregulation of osteoclast differentiation, maturation, and activity, but few OPN-containing cells may prove the common disregulation of bone remodelling during cleft morphopathogenesis.

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“…A number of in vitro tests, pre-clinical and clinical studies also provide evidence of the involvement of OPG in the immune system. 6 Studies have shown that OPG has a central role in immune response and may mediate cell survival. Yun et al 47 showed that OPG regulates B-cell maturation, as mice lacking OPG have a higher population of these cells.…”

Section: Osteoprotegerin and Cardiovascular Diseasementioning

confidence: 99%

“…5 OPG was identified as a cytokine member of the TNF receptor superfamily that binds to two ligands, the receptor activator of nuclear factor kappa-B ligand (RANKL), a key cytokine for the differentiation of osteoclasts, and a ligand related to the induction of apoptosis (TRAIL), involved in immune surveillance. 6 After binding to the first ligand, OPG inhibits the activation of osteoclasts, while the binding between OPG and TRAIL prevents apoptosis of tumor cells. Thus, as a decoding receiver for RANKL and TRAIL, OPG inhibits the regulation effects of nuclear factor kB on inflammation, and on the skeletal and vascular systems, preventing apoptosis induced by TRAIL.…”

Section: Osteoprotegerin (Opg)mentioning

confidence: 99%