Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.

Estrogen plays an important role in the maintenance of bone formation, and deficiency in the production of estrogen is directly linked to postmenopausal osteoporosis. To date, the underlying mechanisms of estrogen-mediated osteogenic differentiation are not well understood. In this study, a pluripot...

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Autores principales: Jinlan Gao, Qi Liu, Xing Liu, Chunyan Ji, Shengqiang Qu, Shusen Wang, Yang Luo
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Publicado: Public Library of Science (PLoS) 2014
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Acceso en línea:https://doaj.org/article/1ad949283bde4278bd3b945c5355fcb5
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spelling oai:doaj.org-article:1ad949283bde4278bd3b945c5355fcb52021-11-18T08:29:57ZCyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.1932-620310.1371/journal.pone.0089884https://doaj.org/article/1ad949283bde4278bd3b945c5355fcb52014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24595300/?tool=EBIhttps://doaj.org/toc/1932-6203Estrogen plays an important role in the maintenance of bone formation, and deficiency in the production of estrogen is directly linked to postmenopausal osteoporosis. To date, the underlying mechanisms of estrogen-mediated osteogenic differentiation are not well understood. In this study, a pluripotent mesenchymal precursor cell line C2C12 was used to induce osteogenic differentiation and subjected to detection of gene expressions or to manipulation of cyclin G2 expressions. C57BL/6 mice were used to generate bilateral ovariectomized and sham-operated mice for analysis of bone mineral density and protein expression. We identified cyclin G2, an unconventional member of cyclin, is involved in osteoblast differentiation regulated by estrogen in vivo and in vitro. In addition, the data showed that ectopic expression of cyclin G2 suppressed expression of osteoblast transcription factor Runx2 and osteogenic differentiation marker genes, as well as ALP activity and in vitro extracellular matrix mineralization. Mechanistically, Wnt/β-catenin signaling pathway is essential for cyclin G2 to inhibit osteogenic differentiation. To the best of our knowledge, the current study presents the first evidence that cyclin G2 serves as a negative regulator of both osteogenesis and Wnt/β-catenin signaling. Most importantly, the basal and 17β-estradiol-induced osteogenic differentiation was restored by overexpression of cyclin G2. These results taken together suggest that cyclin G2 may function as an endogenous suppressor of estrogen-induced osteogenic differentiation through inhibition of Wnt/β-catenin signaling.Jinlan GaoQi LiuXing LiuChunyan JiShengqiang QuShusen WangYang LuoPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 3, p e89884 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Jinlan Gao
Qi Liu
Xing Liu
Chunyan Ji
Shengqiang Qu
Shusen Wang
Yang Luo
Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
description Estrogen plays an important role in the maintenance of bone formation, and deficiency in the production of estrogen is directly linked to postmenopausal osteoporosis. To date, the underlying mechanisms of estrogen-mediated osteogenic differentiation are not well understood. In this study, a pluripotent mesenchymal precursor cell line C2C12 was used to induce osteogenic differentiation and subjected to detection of gene expressions or to manipulation of cyclin G2 expressions. C57BL/6 mice were used to generate bilateral ovariectomized and sham-operated mice for analysis of bone mineral density and protein expression. We identified cyclin G2, an unconventional member of cyclin, is involved in osteoblast differentiation regulated by estrogen in vivo and in vitro. In addition, the data showed that ectopic expression of cyclin G2 suppressed expression of osteoblast transcription factor Runx2 and osteogenic differentiation marker genes, as well as ALP activity and in vitro extracellular matrix mineralization. Mechanistically, Wnt/β-catenin signaling pathway is essential for cyclin G2 to inhibit osteogenic differentiation. To the best of our knowledge, the current study presents the first evidence that cyclin G2 serves as a negative regulator of both osteogenesis and Wnt/β-catenin signaling. Most importantly, the basal and 17β-estradiol-induced osteogenic differentiation was restored by overexpression of cyclin G2. These results taken together suggest that cyclin G2 may function as an endogenous suppressor of estrogen-induced osteogenic differentiation through inhibition of Wnt/β-catenin signaling.
format article
author Jinlan Gao
Qi Liu
Xing Liu
Chunyan Ji
Shengqiang Qu
Shusen Wang
Yang Luo
author_facet Jinlan Gao
Qi Liu
Xing Liu
Chunyan Ji
Shengqiang Qu
Shusen Wang
Yang Luo
author_sort Jinlan Gao
title Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
title_short Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
title_full Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
title_fullStr Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
title_full_unstemmed Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling.
title_sort cyclin g2 suppresses estrogen-mediated osteogenesis through inhibition of wnt/β-catenin signaling.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/1ad949283bde4278bd3b945c5355fcb5
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AT xingliu cycling2suppressesestrogenmediatedosteogenesisthroughinhibitionofwntbcateninsignaling
AT chunyanji cycling2suppressesestrogenmediatedosteogenesisthroughinhibitionofwntbcateninsignaling
AT shengqiangqu cycling2suppressesestrogenmediatedosteogenesisthroughinhibitionofwntbcateninsignaling
AT shusenwang cycling2suppressesestrogenmediatedosteogenesisthroughinhibitionofwntbcateninsignaling
AT yangluo cycling2suppressesestrogenmediatedosteogenesisthroughinhibitionofwntbcateninsignaling
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