Diphlorethohydroxycarmalol from Ishige okamurae Suppresses Osteoclast Differentiation by Downregulating the NF-κB Signaling Pathway

Ihn, Hye Jung; Kim, Ju Ang; Cho, Hye Sung; Shin, Hong‐In; Kim, Gi‐Young; Choi, Yung Hyun; Jeon, You‐Jin; Park, Eui Kyun

doi:10.3390/ijms18122635

Cited by 17 publications

(16 citation statements)

References 29 publications

(32 reference statements)

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“…RANK is located in the cell membrane of osteoclasts and facilitates osteoclast activation and differentiation . RANKL was declared to accelerate bone resorption and depression of NF‐κB pathway represses osteoclast differentiation . All the above demonstrations provided evidence that the NF‐κB pathway plays an important role in OP progression and makes simulative effects on bone resorption and activation of OP.…”

Section: Discussionmentioning

confidence: 90%

“…3 RANKL was declared to accelerate bone resorption and depression of NF-κB pathway represses osteoclast differentiation. 36,37 All the above demonstrations provided evidence that the NF-κB pathway plays an important role in OP progression and makes simulative effects on bone resorption and activation of OP. In the present study, we found that the NF-κB pathway could be inhibited by CST5 up-regulation and by which mechanism the progression of OP was impeded.…”

Section: Discussionmentioning

confidence: 91%

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Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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Here, we aim at exploring the effect of CST5 on bone resorption and activation of osteoclasts in osteoporosis (OP) rats through the NF‐κB pathway. Microarray analysis was used to screen the OP‐related differentially expressed genes. Osteoporosis was induced in rats by intragastric retinoic acid administration. The serum levels of tartrate‐resistant acid phosphatase (TRAP), bone alkaline phosphatase (BALP) and osteocalcin (OC) and the expression of CD61 on the surface of osteoclasts were examined. The number of osteoclasts and the number and area of resorption pits were detected. Besides, the pathological changes and bone mineral density in bone tissues of rats were assessed. Also, the relationship between CST5 and the NF‐κB pathway was identified through determining the expression of CST5, RANKL, RANK, OPG, p65 and IKB. Poorly expressed CST5 was indicated to affect the OP. CST5 elevation and inhibition of the NF‐κB pathway decreased serum levels of TRAP, BALP and OC and expression of CD61 in vivo and in vitro. In OP rats, CST5 overexpression increased trabecular bones and bone mineral density of bone tissues, but decreased trabecular separation, fat within the bone marrow cavities and the number of osteoclasts through inhibiting the NF‐κB pathway. In vivo experiments showed that CST5 elevation inhibited growth in number and area of osteoclastic resorption pits and restrained osteoclastic bone absorption by inhibiting the NF‐κB pathway. In summary, overexpression of CST5 suppresses the activation and bone resorption of osteoclasts by inhibiting the activation of the NF‐κB pathway.

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 91%

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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show abstract

“…RANKL/RANK/osteoprotegerin (OPG) signaling plays a critical role in bone remodeling and suppression and this is effective in various bone diseases with increased bone loss in animal models [18]. Recently, diphlorethohydroxycarmalol, a phlorotanin isolated from brown alga (Ishige okamurae) brought about an antiosteoclastogenetic effect by suppressing RANKL/NF-κB signaling [19].…”

Section: Effect Of Ece On Osteoclast Differentiation and Bone Resorptmentioning

confidence: 99%

Ecklonia cava Extract Containing Dieckol Suppresses RANKL-Induced Osteoclastogenesis via MAP Kinase/NF-��B Pathway Inhibition and Heme Oxygenase-1 Induction

Kim

Kang

Choi

et al. 2019

Journal of Microbiology and Biotechnology

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Ecklonia cava, an edible marine brown alga (Laminariaceae), is a rich source of bioactive compounds such as fucoidan and phlorotannins. Ecklonia cava extract (ECE) was prepared using 70% ethanol extraction and ECE contained 67% and 10.6% of total phlorotannins and dieckol, respectively. ECE treatment significantly inhibited receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation of RAW 264.7 cells and pit formation in bone resorption assay (p <0.05). Moreover, it suppressed RANKL-induced NF-κB and mitogen-activated protein kinase signaling in a dose dependent manner. Downregulated osteoclast-specific gene (tartrate-resistant acid phosphatase, cathepsin K, and matrix metalloproteinase-9) expression and osteoclast proliferative transcriptional factors (nuclear factor of activated T cells-1 and c-fos) confirmed ECE-mediated suppression of osteoclastogenesis. ECE treatment (100 μg/ml) increased heme oxygenase-1 expression by 2.5-fold and decreased intercellular reactive oxygen species production during osteoclastogenesis. The effective inhibition of RANKL-stimulated osteoclast differentiation and oxidative stress by ECE suggest that ECE has therapeutic potential in alleviating osteoclast-associated disorders.

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“…Additionally, phosphorylation of phospholipase Cc (PLCc) activates the Ca 2þ /NFATc1 signalling pathway, which is important in osteoclastogenesis [7]. RANKL also induces the expression of tartrate-resistant acid phosphatase (TRAP), which is a marker gene of osteoclastogenesis [8]. The regulatory mechanisms of osteoclast differentiation are complex.…”

Section: Introductionmentioning

confidence: 99%

Cysteinyl leukotriene receptor 1 (cysLT1R) regulates osteoclast differentiation and bone resorption

Zheng

Shi

2018

Artificial Cells, Nanomedicine, and Biotechnology

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Excessive bone resorption induced by abnormal osteoclast differentiation has been associated with bone microstructure damage and bone-associated disorders, including osteoporosis. Here, we investigated the physiological roles of the type 1 cysteinyl leukotriene receptor (cysLTR-1) and the pharmacological functions of the specific cysLTR-1 antagonist montelukast on M-CSF- and RANKL-induced osteoclast differentiation. We showed that cysLTR-1 but not cysLTR-2 is expressed in osteoclast precursor cells: mouse bone marrow-derived macrophages (BMMs). We also found that treatment with M-CSF and RANKL significantly increased expression of cysLTR-1. Overexpression of cysLTR-1 promoted osteoclast differentiation of BMMs by increasing NFATc1 and TRAP. In contrast, treatment with montelukast prevented M-CSF- and RANKL-induced osteoclast differentiation of BMMs. Mechanically, our findings demonstrate that montelukast treatment attenuated activation of the ERK1/2, p38, JNK and NF-κB signalling pathways. Additionally, we reported that montelukast treatment ameliorated the generation of ROS and calcium signalling. Importantly, the co-immunoprecipitation assay displayed that montelukast treatment prevented the interaction of RANK and TRAF6. Finally, in vivo experiments indicated that montelukast rescued the reduction of bone volume as well as trabecular number in an ovariectomy mouse model.

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Diphlorethohydroxycarmalol from Ishige okamurae Suppresses Osteoclast Differentiation by Downregulating the NF-κB Signaling Pathway

Cited by 17 publications

References 29 publications

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Ecklonia cava Extract Containing Dieckol Suppresses RANKL-Induced Osteoclastogenesis via MAP Kinase/NF-��B Pathway Inhibition and Heme Oxygenase-1 Induction

Cysteinyl leukotriene receptor 1 (cysLT1R) regulates osteoclast differentiation and bone resorption

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