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Int. J. Mol. Sci. 2017, 18(3), 581; doi:10.3390/ijms18030581

Methyl Gallate Inhibits Osteoclast Formation and Function by Suppressing Akt and Btk-PLCγ2-Ca2+ Signaling and Prevents Lipopolysaccharide-Induced Bone Loss

1
Department of Anatomy, School of Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, Korea
2
Imaging Science-based Lung and Bone Diseases Research Center, Wonkwang University, Iksan, Jeonbuk 570-749, Korea
3
Department of Radiology, School of Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, Korea
4
Division of Rheumatology, Department of Internal Medicine, Wonkwang University, Iksan, Jeonbuk 570-749, Korea
*
Author to whom correspondence should be addressed.
Academic Editor: Cory J. Xian
Received: 17 January 2017 / Revised: 1 March 2017 / Accepted: 2 March 2017 / Published: 7 March 2017
(This article belongs to the Special Issue Advances in Bone and Cartilage Research)
View Full-Text   |   Download PDF [2786 KB, uploaded 7 March 2017]   |  

Abstract

In the field of bone research, various natural derivatives have emerged as candidates for osteoporosis treatment by targeting abnormally elevated osteoclastic activity. Methyl gallate, a plant-derived phenolic compound, is known to have numerous pharmacological effects against inflammation, oxidation, and cancer. Our purpose was to explore the relation between methyl gallate and bone metabolism. Herein, we performed screening using methyl gallate by tartrate resistant acid phosphatase (TRAP) staining and revealed intracellular mechanisms responsible for methyl gallate-mediated regulation of osteoclastogenesis by Western blotting and quantitative reverse transcription polymerase chain reaction (RT-PCR). Furthermore, we assessed the effects of methyl gallate on the characteristics of mature osteoclasts. We found that methyl gallate significantly suppressed osteoclast formation through Akt and Btk-PLCγ2-Ca2+ signaling. The blockade of these pathways was confirmed through transduction of cells with a CA-Akt retrovirus and evaluation of Ca2+ influx intensity (staining with Fluo-3/AM). Indeed, methyl gallate downregulated the formation of actin ring-positive osteoclasts and resorption pit areas. In agreement with in vitro results, we found that administration of methyl gallate restored osteoporotic phenotype stimulated by acute systemic injection of lipopolysaccharide in vivo according to micro-computed tomography and histological analysis. Our data strongly indicate that methyl gallate may be useful for the development of a plant-based antiosteoporotic agent. View Full-Text
Keywords: methyl gallate; osteoclast; Akt; Ca2+ signaling; bone resorption; osteoporosis methyl gallate; osteoclast; Akt; Ca2+ signaling; bone resorption; osteoporosis
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MDPI and ACS Style

Baek, J.M.; Kim, J.-Y.; Lee, C.H.; Yoon, K.-H.; Lee, M.S. Methyl Gallate Inhibits Osteoclast Formation and Function by Suppressing Akt and Btk-PLCγ2-Ca2+ Signaling and Prevents Lipopolysaccharide-Induced Bone Loss. Int. J. Mol. Sci. 2017, 18, 581.

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