Dehydrodiconiferyl alcohol promotes BMP-2-induced osteoblastogenesis through its agonistic effects on estrogen receptor

Lee, Wonwoo; Ko, Kyeong Ryang; Kim, Hyun-keun; Lim, Seonung; Kim, Sun‐Young

doi:10.1016/j.bbrc.2017.12.079

Cited by 22 publications

(14 citation statements)

References 29 publications

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“…The mineralization in the autocrine or paracrine pathway within osteoblasts can also be induced by type I adiponectin receptor and the AMPK signaling pathway. Lee found that the differentiation of osteoblasts induced by BMP could be blocked by Compound C, accompanied by the downregulation of osteogenic marker genes, including Runx2, Osx , and Ocn [ 39 ]. Acetyl-coA carboxylase (ACC) is an important down-stream enzyme of AMPK involved in the regulation of bone metabolism [ 40 ].…”

Section: Discussionmentioning

confidence: 99%

Trelagliptin stimulates osteoblastic differentiation by increasing runt-related transcription factor 2 (RUNX2): a therapeutic implication in osteoporosis

Shao

Cao

et al. 2021

Bioengineered

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Osteoporosis, an aging-associated bone metabolic disease, is affecting millions of people worldwide. The deregulated process of osteoblastic differentiation has been linked with the progression of osteoporosis. Trelagliptin is a long-acting inhibitor of DPP-4 used for the management of type 2 diabetes mellitus. However, it is unknown whether Trelagliptin possesses a beneficial effect in osteoblastic differentiation. Interestingly, we found that treatment with Trelagliptin enhanced differentiation and promoted the mineralization of MC3T3-E1 cells. Firstly, Trelagliptin increased the activity of alkaline phosphatase (ALP) and promoted osteoblastic calcium deposition. Additionally, treatment with Trelagliptin upregulated ALP, osteocalcin (OCN), osteopontin (OPN), and bone morphogenetic protein-2 (BMP-2). Notably, Trelagliptin increased RUNX2, a major regulator of osteoblastic differentiation. Mechanistically, Trelagliptin upregulated the levels of p-AMPKα. Blockage of AMPK with compound C abolished the effects of Trelagliptin in RUNX2 and osteoblastic differentiation, suggesting the involvement of AMPK. Our findings suggest that Trelagliptin might possess a potential for the treatment of osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Trelagliptin stimulates osteoblastic differentiation by increasing runt-related transcription factor 2 (RUNX2): a therapeutic implication in osteoporosis

Shao

Cao

et al. 2021

Bioengineered

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“…Studies have shown that cytokine sensitivity screening considers the BMP4 signaling pathway to be crucial for treating ER + breast cancer ( Shee et al, 2019 ). In addition, dehydrodiconiferyl alcohol has been found to promote BMP-2-induced osteoblastogenesis through its agonistic effects on estrogen receptors ( Lee et al, 2018 ). In their study, Pang et al found that quercetin stimulates BMSC differentiation through an estrogen receptor-mediated pathway ( Pang et al, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

β-Ecdysterone Enhanced Bone Regeneration Through the BMP-2/SMAD/RUNX2/Osterix Signaling Pathway

Yan

Wang

Jiang

et al. 2022

Front. Cell Dev. Biol.

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Graphical AbstractSchematic illustrations of the fabrication of the bone defect model and action of β-Ecd in promoting bone regeneration and repair of bone defects. We established a rat model of a femoral bone defect in vivo to evaluate the effect of β-Ecd on bone regeneration. Rats injected intraperitoneally with 72 mg/kg β-Ecd showed a higher degree of ossification of regenerated bone tissue at the site of the bone defect at weeks 4 and 8. β-ecdysterone binding to the BMP2 receptor activates SMAD1 to bind to SMAD1/5/8, promotes RUNX2 and OSTERIX replication in the nucleus, and mediates bone regeneration. This study provides a new approach to the treatment of bone injury and degenerative diseases represented by bone defects and osteoporosis.

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“…Luciferase reporter plasmid containing the inducible xenobiotic response element (XRE), which directly interact with the aryl hydrocarbon receptor (AhR), was purchased from QIAGEN (Valencia, CA, USA). A reporter plasmid assay was conducted, as described previously [34,35]. Briefly, HaCaT cells were transiently transfected with an XRE-reporter plasmid and a β-galactosidase plasmid (Invitrogen, Carlsbad, CA, USA), using lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) following the manufacturer’s protocol.…”

Section: Methodsmentioning

confidence: 99%

Water-Soluble Extract from Actinidia arguta (Siebold & Zucc.) Planch. ex Miq. and Perilla frutescens (L.) Britton, ACTPER, Ameliorates a Dry Skin-Induced Itch in a Mice Model and Promotes Filaggrin Expression by Activating the AhR Signaling in HaCaT Cells

et al. 2019

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With a complex etiology involving multiple factors, the condition known as itch is a primary symptom of many skin diseases. Current treatment methods are ineffective for addressing itches caused by dry skin, for example. We developed a botanical extract, ACTPER, made from a mixture of Actinidia arguta and Perilla frutescens, which have traditionally been used to treat itch. The quality of ACTPER as a research agent was controlled in our experiment by cell-based bioassays, as well as by high-performance liquid chromatography (HPLC), using two chemical markers. In the acetone-induced dry skin mice model, the oral administration of ACTPER alleviated dry skin-related skin properties and itching behavior. The RNA and protein expression of the filament aggregating protein (filaggrin) gene, a key factor involved in the regulation of skin barrier function, was significantly increased, as measured by quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence assay. To understand the underlying mechanism(s) at the molecular level, HaCaT cells, a human keratinocyte-derived cell line, were treated with various concentrations of ACTPER. We found that the protein expression of filaggrin was indeed upregulated by ACTPER in a dose dependent manner. Data from experiments involving the reporter plasmid containing the xenobiotic response element (XRE), and the chemical antagonist for the aryl hydrocarbon receptor (AhR), indicated that the ACTPER-mediated upregulation of filaggrin was controlled through the activation of the AhR signaling pathway. The molecular docking simulation study predicted that ACTPER might contain chemical compounds that bind directly to AhR. Taken together, our results suggest that ACTPER may provide the platform, based upon which a variety of safe and effective therapeutic agents can be developed to treat itch.

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Dehydrodiconiferyl alcohol promotes BMP-2-induced osteoblastogenesis through its agonistic effects on estrogen receptor

Cited by 22 publications

References 29 publications

Trelagliptin stimulates osteoblastic differentiation by increasing runt-related transcription factor 2 (RUNX2): a therapeutic implication in osteoporosis

Trelagliptin stimulates osteoblastic differentiation by increasing runt-related transcription factor 2 (RUNX2): a therapeutic implication in osteoporosis

β-Ecdysterone Enhanced Bone Regeneration Through the BMP-2/SMAD/RUNX2/Osterix Signaling Pathway

Water-Soluble Extract from Actinidia arguta (Siebold & Zucc.) Planch. ex Miq. and Perilla frutescens (L.) Britton, ACTPER, Ameliorates a Dry Skin-Induced Itch in a Mice Model and Promotes Filaggrin Expression by Activating the AhR Signaling in HaCaT Cells

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