(−)-Epigallocatechin gallate but not chlorogenic acid upregulates osteoprotegerin synthesis through regulation of bone morphogenetic protein-4 in osteoblasts

Fujita, Kazuo; Otsuka, Takanobu; Yamamoto, Naohiro; Kainuma, Shingo; Ohguchi, Reou; Kawabata, Tetsu; Sakai, Go; Kuroyanagi, Gen; Matsushima‐Nishiwaki, Rie; Kozawa, Osamu; Tokuda, Harukuni

doi:10.3892/etm.2017.4491

Cited by 11 publications

(13 citation statements)

References 30 publications

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“…Furthermore, Fujita et al. revealed that BMP‐4 stimulated OPG synthesis in osteoblast cells independent from other pathways such as Smad1 or p38 MAPK . Increased levels observed in the present study might also indicate increased osteoblastic activity.…”

Section: Discussionsupporting

confidence: 61%

Evaluation of the effect of oleuropein on alveolar bone loss, inflammation, and apoptosis in experimental periodontitis

Taşkan

Yüce

Karataş

et al. 2019

J of Periodontal Research

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The Objective The present study aimed to evaluate the effects of oleuropein on ligature‐induced alveolar bone loss. In this respect, osteoblastic activity, osteoclastic activity, inflammatory markers, and apoptosis were evaluated. Background Oleuropein is a flavonoid, which has potent anti‐inflammatory and bone‐protective effects. Methods Thirty‐two Wistar rats were divided into four experimental groups as following: control (C, n = 8) group; periodontitis (P, n = 8) group; periodontitis and low‐dose oleuropein group (12 mg/kg/day oleuropein, LDO group, n = 8); and periodontitis and high‐dose oleuropein group (24 mg/kg/day oleuropein, HDO group, n = 8). Periodontitis was induced via ligatures. Study period was 14 days, and animals were sacrificed at end of this period. Mandibles were examined via a stereomicroscope and underwent histological procedures. Osteoblast, tartrate‐resistant acid phosphatase (TRAP)‐positive osteoclast, and inflammatory cell counts were determined in hematoxylin‐eosin stained sections. Inducible nitric oxide synthase (iNOS), bone morphogenetic protein‐4, the cluster of differentiation (CD)‐68, cysteine‐aspartic proteases‐3 (Caspase 3), and B‐cell lymphoma‐2 (Bcl‐2) expressions were evaluated via immunohistochemistry. Results Periodontitis group had highest alveolar bone loss, and these levels significantly decreased in LDO and HDO groups. Both 12 and 24 mg/kg oleuropein groups significantly increased osteoblast cell counts and decreased TRAP‐positive osteoclast and inflammatory cell counts. BMP‐4 and bcl‐2 expressions were elevated in oleuropein groups while caspase‐3 expressions decreased. iNOS and CD68 were higher in periodontitis group compared to control group, but there was no significant difference between other groups. Conclusion Oleuropein successfully decreased alveolar bone loss as a result of decreased osteoclastic activity, inflammation, and apoptosis and increased osteoblastic activity.

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Section: Discussionsupporting

confidence: 61%

Evaluation of the effect of oleuropein on alveolar bone loss, inflammation, and apoptosis in experimental periodontitis

Taşkan

Yüce

Karataş

et al. 2019

J of Periodontal Research

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“…We realized that Shh and AKT signaling pathways might be not the only signaling pathways underlying the effect of EGCG. Other signaling pathways, such as Wnt, Notch and bone morphogenetic protein, are implicated in the development of hair follicles ( Rishikaysh et al, 2014 ) and influenced by EGCG in several other reports ( Jin et al, 2013 ; Fujita et al, 2017 ; Zhu et al, 2017 ). Thus, these signaling pathways may be also involved in the growth-promoting effect of EGCG on mink hair follicle growth, but more explorations are needed.…”

Section: Discussionmentioning

confidence: 99%

Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

et al. 2018

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Background: Hair follicles play an essential role in the growth of hair. Epigallocatechin-3-gallate (EGCG), a catechin polyphenol in green tea, has various bioactivities. The present study aims to evaluate the effect of EGCG on the growth of mink hair follicles and investigate the possible molecular mechanisms.Methods: The length of hair follicles was recorded up to 6 days in presence of 0.1–5 μM EGCG. Primary dermal papilla cells (DPCs) and outer root sheath cells (ORSCs) were treated with 0.25–4 μM EGCG, and their growth was evaluated by MTT assay and cell cycle detection. The levels of key molecules in sonic hedgehog (Shh) and protein kinase B (AKT) signaling pathways were further assessed by quantitative real-time PCR, western blot and immunofluorescence. To determine the involvement of Shh and AKT pathways in EGCG-mediated growth-promotion of ORSCs and DPCs, Shh pathway inhibitors cyclopamine and GANT61 or AKT pathway inhibitor LY294002 were employed, and then cell proliferation and cell cycle were analyzed.Results: Data from ex vivo culture showed that, in presence of 0.5–2.5 μM EGCG, the growth of mink hair follicles was promoted. In vitro, the proliferation of DPCs and ORSCs was enhanced by 0.5–4 μM EGCG treatment. More cells entered S phase upon treatment of EGCG, accompanied with upregulation of cyclin D1 and cyclin E1. Furthermore, when exposed to EGCG, the Shh and AKT signaling pathways were activated in both hair follicles and primary DPCs and ORSCs. Inhibiting either of these two pathways partly reversed the effect of EGCG on proliferation and cell cycle of DPCs and ORSCs.Conclusion: EGCG promotes the growth of mink hair follicles at concentrations of 0.5–2.5 μM. This growth-promoting effect of EGCG may be associated with the increased proliferation of DPCs and ORSCs through activating Shh and AKT signaling pathways.

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“…It has further been reported that EGCG may inhibit osteoclastic bone resorption and stimulate osteoblastic TETSU KAWABATA 1-3 , HARUHIKO TOKUDA 2,4 , GO SAKAI 1,2 , KAZUHIKO FUJITA 1,2 , RIE MATSUSHIMA-NISHIWAKI 2 , TAKANOBU OTSUKA 1 and OSAMU KOZAWA 2 bone formation (18,19). In our previous study (20), it was identified that EGCG enhanced osteoprotegerin synthesis in osteoblast-like MC3T3-E1 cells. However, the exact roles of chlorogenic acid and EGCG in bone metabolism are yet to be fully clarified.…”

Section: Introductionmentioning

confidence: 85%

Repression of IGF-I-induced osteoblast migration by (-)-epigallocatechin gallate through p44/p42 MAP kinase signaling

et al. 2018

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Polyphenolic compounds in beverages may have benefits in the prevention of osteoporosis. It has been demonstrated previously that insulin-like growth factor-I (IGF-I) could stimulate the migration of osteoblasts. In the present study, it was investigated whether chlorogenic acid, a major polyphenol in coffee, and (-)-epigallocatechin gallate (EGCG), a major polyphenol in green tea, could affect this IGF-I-stimulated migration of osteoblast-like MC3T3-E1 cells. The IGF-I-stimulated osteoblast migration, evaluated by Transwell cell migration and wound-healing assays, was inhibited by EGCG but not chlorogenic acid. IGF-I induced the phosphorylation of p44/p42 mitogen-activated protein (MAP) kinase, p70 S6 kinase and Akt. The IGF-I-induced migration was suppressed by PD98059, a MAP kinase kinase 1/2 inhibitor, and deguelin, an Akt inhibitor, but not rapamycin, an inhibitor of the upstream kinase of p70 S6 kinase (mammalian target of rapamycin). EGCG attenuated the IGF-I-induced phosphorylation of p44/p42 MAP kinase but not Akt. Taken together, the present results suggest that EGCG inhibits IGF-I-induced osteoblast migration via p44/p42 MAP kinase.

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(−)-Epigallocatechin gallate but not chlorogenic acid upregulates osteoprotegerin synthesis through regulation of bone morphogenetic protein-4 in osteoblasts

Cited by 11 publications

References 30 publications

Evaluation of the effect of oleuropein on alveolar bone loss, inflammation, and apoptosis in experimental periodontitis

Evaluation of the effect of oleuropein on alveolar bone loss, inflammation, and apoptosis in experimental periodontitis

Epigallocatechin-3-Gallate Promotes the Growth of Mink Hair Follicles Through Sonic Hedgehog and Protein Kinase B Signaling Pathways

Repression of IGF-I-induced osteoblast migration by (-)-epigallocatechin gallate through p44/p42 MAP kinase signaling

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