Zebrafish scales respond differently to in vitro dynamic and static acceleration: Analysis of interaction between osteoblasts and osteoclasts

Kitamura, Kei-ichiro; Takahira, Koh; Inari, Masato; Satoh, Yusuke; Hayakawa, Kazuichi; Tabuchi, Yoshiaki; Ogai, Kazuhiro; Nishiuchi, Takumi; Kondo, Takashi; Mikuni-Takagaki, Yuko; Chen, Wenxi; Hattori, Atsuhiko; Suzuki, Nobuo

doi:10.1016/j.cbpa.2013.04.023

Cited by 33 publications

(24 citation statements)

References 22 publications

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“…Homologous forms of RANK, RANKL and OPG have been found in fish suggesting a conservation of the crosstalk pathway between osteoblast and osteoclast (Kitamura et al . ). In our GIOP model, GC could stimulate active osteoblasts to produce RANKL which, in turn, stimulate the recruited osteoclastic precursors to differentiate in loco .…”

Section: Discussionmentioning

confidence: 97%

Alendronate rescued osteoporotic phenotype in a model of glucocorticoid‐induced osteoporosis in adult zebrafish scale

Pasqualetti

Congiu

Banfi

et al. 2015

Int J Experimental Path

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Long-term effects of glucocorticoid treatment in humans induce bone loss and increase the risk of fracture in the skeleton. The pathogenic mechanisms of glucocorticoid-induced osteoporosis (GIOP) are still unclear. The GIOP and its effects have been reproduced in several animal models including Danio rerio (zebrafish) embryo. The treatment of adult fish with prednisolone (PN) has shown a dose-dependent decrease of mineralized matrix in the scales. Large resorption lacunae are characterized by single TRAP-positive cells which migrate to the margin of the scale merging into a multinucleated structures. The treatment with PN of cultured scales did not increase TRAP activity suggesting that the massive presence of osteoclasts in the resorption sites could be likely the result of a systemic recruitment of monocyte-macrophage precursors. We observed that treatment with PN induced a significant decrease of the alkaline phosphatase (ALP) activity in scale scleroblasts if compared with untreated controls. Then, we investigated the total mineral balance under prednisolone treatment using a time-dependent double live staining. The untreated fish fully repaired the resorption lacuna induced by prednisolone, whereas treated fish failed. The presence of osteoclast resorption fingerprints on new matrix suggested that the osteoclast activity counterbalances the osteodepositive activity exerted by scleroblasts. The treatment with PN in association with alendronate (AL) has surprisingly resulted in a significant decrease of TRAP activity and increase of ALP compared to PN-treated fish in biochemical and histological assays confirming the action of alendronate against GIOP in fish as well in humans.

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Section: Discussionmentioning

confidence: 97%

Alendronate rescued osteoporotic phenotype in a model of glucocorticoid‐induced osteoporosis in adult zebrafish scale

Pasqualetti

Congiu

Banfi

et al. 2015

Int J Experimental Path

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“…26 RANKL binds to the osteoclast surface receptor RANK, promotes osteoclast formation, differentiation, maturation, inhibits osteoclast apoptosis, and prolongs its survival. 27,28 OPG prevents RANKL and RANK interaction by binding to RANKL in adjacent osteoclasts, thereby inhibiting osteoclast formation, differentiation, survival, activation, and induction of osteoclast apoptosis. 29 Study has shown that the analysis of OPG/RANKL ratio can re ect the osteogenic effect, osteoclast effect and bone turnover state.…”

Section: Discussionmentioning

confidence: 99%

Icariin Combined with Adipose-Derived Stem Cells Ameliorated Osteoporosis in Postmenopausal Rats

Sun¹,

Wang²,

Tang³

et al. 2020

Preprint

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Purpose: Osteoporosis is a chronic metabolic disease, it has caused the high incidence of related fractures, which seriously affects the life quality of the patients, especially in early postmenopausal women. Methods: Rat osteoporosis model was induced by bilateral ovarian ablation. Sprague Dawley (SD) rats were randomly divided into five groups (n=9): sham group, model group, the icariin group, ADSCs group, icariin combined with ADSCs group. H&E staining was used to observe the pathological changes of femur. The expression of calcitonin receptor (CALCR) and cathepsin K (CTSK) were investigated by immunohistochemistry. The expression of osteoprotegerin (OPG) and receptor activator of nuclear factor-κB ligand (RANKL) were measured by qRT-PCR, immunohistochemistry and western blot.Results: The results showed that icariin combined with ADSCs ameliorated osteoblast morphology and bone density. Icariin combined with ADSCs significantly attenuated the protein expression of CALCR and CTSK after ovariectomy. Moreover, the expressions of OPG mRNA and protein were increased (p < 0.05), while the expressions of RANKL mRNA and protein were decreased (p < 0.05) in osteoblasts.Conclusions: Icariin combined with ADSCs can effectively inhibit PMOP in rats. The mechanism may be achieved by up-regulated the ratio of OPG / RANKL.

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“…These cells will express RANKL, which, together with a number of cytokines, activate osteoclastogenesis. Moreover, osteocytes also synthesize osteoprotegerin (a decoy receptor for RANKL), which inhibits interaction between RANKL and RANK and thus inhibits osteoclastogenesis (Kitamura et al 2013, Takahashi et al 2011. Maturation of bone forming osteoblastic cell line is promoted by the canonical pathway of Wnt (wingless proteins), as well as by hormones produced in osteocytes 1,25(OH) 2 D 3 (Turner et al 2014) and BMP-4 (activated by the p38 MAP kinase) (Kondo et al 2014).…”

Section: Involvement Of Osteoblastic Cell Line (Osteocytes) In Regulamentioning

confidence: 99%

Bone Tissue as a Systemic Endocrine Regulator

Žofková

2015

Physiol Res

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Bone is a target tissue for hormones, such as the sex steroids, parathormon, vitamin D, calcitonin, glucocorticoids, and thyroid hormones. In the last decade, other "non-classic" hormones that modulate the bone tissue have been identified. While incretins (GIP and GLP-1) inhibit bone remodeling, angiotensin acts to promote remodeling. Bone morphogenetic protein (BMP) has also been found to have anabolic effects on the skeleton by activating bone formation during embryonic development, as well as in the postnatal period of life. Bone has also been identified as an endocrine tissue that produces a number of hormones, that bind to and modulate extra-skeletal receptors. Osteocalcin occupies a central position in this context. It can increase insulin secretion, insulin sensitivity and regulate metabolism of fatty acids. Moreover, osteocalcin also influences phosphate metabolism via osteocyte-derived FGF23 (which targets the kidneys and parathyroid glands to control phosphate reabsorption and metabolism of vitamin D). Finally, osteocalcin stimulates testosterone synthesis in Leydig cells and thus may play some role in male fertility. Further studies are necessary to confirm clinically important roles for skeletal tissue in systemic regulations.

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Zebrafish scales respond differently to in vitro dynamic and static acceleration: Analysis of interaction between osteoblasts and osteoclasts

Cited by 33 publications

References 22 publications

Alendronate rescued osteoporotic phenotype in a model of glucocorticoid‐induced osteoporosis in adult zebrafish scale

Alendronate rescued osteoporotic phenotype in a model of glucocorticoid‐induced osteoporosis in adult zebrafish scale

Icariin Combined with Adipose-Derived Stem Cells Ameliorated Osteoporosis in Postmenopausal Rats

Bone Tissue as a Systemic Endocrine Regulator

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