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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| creator | Gao, Jinlan Liu, Qi Liu, Xing Ji, Chunyan Qu, Shengqiang Wang, Shusen Luo, Yang |
| 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. |
| doi_str_mv | 10.1371/journal.pone.0089884 |
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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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0089884</identifier><identifier>PMID: 24595300</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>17β-Estradiol ; Adipocytes ; Animals ; Antibiotics ; Apoptosis ; beta Catenin - metabolism ; Biocompatibility ; Biology ; Biomedical materials ; Bone Density ; Bone growth ; Bone mineral density ; Breast cancer ; Cbfa-1 protein ; Cell cycle ; Cell growth ; Cyclin G2 - physiology ; Differentiation ; Ectopic expression ; Education ; Estrogens ; Estrogens - physiology ; Extracellular matrix ; Female ; Gastric cancer ; Gene expression ; Genomics ; Growth factors ; Inhibition ; Kinases ; Laboratories ; Medicine ; Mesenchyme ; Mice ; Mice, Inbred C57BL ; Mineralization ; Osteoblastogenesis ; Osteogenesis ; Osteogenesis - physiology ; Osteoporosis ; Ovariectomy ; Pluripotency ; Post-menopause ; Proteins ; Public health ; Sex hormones ; Signal transduction ; Signaling ; Stem cells ; Stomach cancer ; Tumor necrosis factor-TNF ; Wnt protein ; Wnt Proteins - metabolism ; β-Catenin</subject><ispartof>PloS one, 2014-03, Vol.9 (3), p.e89884-e89884</ispartof><rights>2014 Gao et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Gao et al 2014 Gao et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-22d93e616be5c3d85c78b8ace00c414024991737fe8b671f67744b7bf033e6273</citedby><cites>FETCH-LOGICAL-c526t-22d93e616be5c3d85c78b8ace00c414024991737fe8b671f67744b7bf033e6273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940656/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940656/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,725,778,782,862,883,2098,2917,23849,27907,27908,53774,53776,79351,79352</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24595300$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Shi, Xing-Ming</contributor><creatorcontrib>Gao, Jinlan</creatorcontrib><creatorcontrib>Liu, Qi</creatorcontrib><creatorcontrib>Liu, Xing</creatorcontrib><creatorcontrib>Ji, Chunyan</creatorcontrib><creatorcontrib>Qu, Shengqiang</creatorcontrib><creatorcontrib>Wang, Shusen</creatorcontrib><creatorcontrib>Luo, Yang</creatorcontrib><title>Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling</title><title>PloS one</title><addtitle>PLoS One</addtitle><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.</description><subject>17β-Estradiol</subject><subject>Adipocytes</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Apoptosis</subject><subject>beta Catenin - metabolism</subject><subject>Biocompatibility</subject><subject>Biology</subject><subject>Biomedical materials</subject><subject>Bone Density</subject><subject>Bone growth</subject><subject>Bone mineral density</subject><subject>Breast cancer</subject><subject>Cbfa-1 protein</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cyclin G2 - physiology</subject><subject>Differentiation</subject><subject>Ectopic expression</subject><subject>Education</subject><subject>Estrogens</subject><subject>Estrogens - physiology</subject><subject>Extracellular matrix</subject><subject>Female</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Genomics</subject><subject>Growth factors</subject><subject>Inhibition</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Medicine</subject><subject>Mesenchyme</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mineralization</subject><subject>Osteoblastogenesis</subject><subject>Osteogenesis</subject><subject>Osteogenesis - physiology</subject><subject>Osteoporosis</subject><subject>Ovariectomy</subject><subject>Pluripotency</subject><subject>Post-menopause</subject><subject>Proteins</subject><subject>Public health</subject><subject>Sex hormones</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Stem cells</subject><subject>Stomach cancer</subject><subject>Tumor necrosis factor-TNF</subject><subject>Wnt protein</subject><subject>Wnt Proteins - metabolism</subject><subject>β-Catenin</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUs1u1DAYjBCIlsIbIIjEhUu2_nd8QUKrtlSqxAXE0bKdL1mvsvZiJ0h9LR6EZ8LbTasWcbL1eWY832iq6i1GK0wlPt_GOQUzrvYxwAqhVrUte1adYkVJIwiizx_dT6pXOW8R4rQV4mV1QhhXnCJ0Wtn1rRt9qK9Inef9PkHOkGvIU4oDhGYHnTcTdHXMExwmkH2up02K87Cpfdh46ycfQx37-keYzv_8blzBh6KY_VDs-TC8rl70ZszwZjnPqu-XF9_WX5qbr1fX6883jeNETA0hnaIgsLDAHe1a7mRrW-MAIccwQ4QphSWVPbRWSNwLKRmz0vaIFhqR9Kx6f9TdjzHrJZ6sMUdUSswlKYjrI6KLZqv3ye9MutXReH03iGnQJk3ejaCx6RRTpKW2A0aKk45axbjjlPPeWV60Pi2_zbak5CBMyYxPRJ--BL_RQ_ylqWJIcFEEPi4CKf6cS-J657ODcTQB4nznm0mGCUUF-uEf6P-3Y0eUSzHnBP2DGYz0oTL3LH2ojF4qU2jvHi_yQLrvCP0LVonAyQ</recordid><startdate>20140303</startdate><enddate>20140303</enddate><creator>Gao, Jinlan</creator><creator>Liu, Qi</creator><creator>Liu, Xing</creator><creator>Ji, Chunyan</creator><creator>Qu, Shengqiang</creator><creator>Wang, Shusen</creator><creator>Luo, Yang</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140303</creationdate><title>Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling</title><author>Gao, Jinlan ; Liu, Qi ; Liu, Xing ; Ji, Chunyan ; Qu, Shengqiang ; Wang, Shusen ; Luo, Yang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-22d93e616be5c3d85c78b8ace00c414024991737fe8b671f67744b7bf033e6273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>17β-Estradiol</topic><topic>Adipocytes</topic><topic>Animals</topic><topic>Antibiotics</topic><topic>Apoptosis</topic><topic>beta Catenin - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gao, Jinlan</au><au>Liu, Qi</au><au>Liu, Xing</au><au>Ji, Chunyan</au><au>Qu, Shengqiang</au><au>Wang, Shusen</au><au>Luo, Yang</au><au>Shi, Xing-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-03-03</date><risdate>2014</risdate><volume>9</volume><issue>3</issue><spage>e89884</spage><epage>e89884</epage><pages>e89884-e89884</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24595300</pmid><doi>10.1371/journal.pone.0089884</doi><oa>free_for_read</oa></addata></record> |
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| subjects | 17β-Estradiol Adipocytes Animals Antibiotics Apoptosis beta Catenin - metabolism Biocompatibility Biology Biomedical materials Bone Density Bone growth Bone mineral density Breast cancer Cbfa-1 protein Cell cycle Cell growth Cyclin G2 - physiology Differentiation Ectopic expression Education Estrogens Estrogens - physiology Extracellular matrix Female Gastric cancer Gene expression Genomics Growth factors Inhibition Kinases Laboratories Medicine Mesenchyme Mice Mice, Inbred C57BL Mineralization Osteoblastogenesis Osteogenesis Osteogenesis - physiology Osteoporosis Ovariectomy Pluripotency Post-menopause Proteins Public health Sex hormones Signal transduction Signaling Stem cells Stomach cancer Tumor necrosis factor-TNF Wnt protein Wnt Proteins - metabolism β-Catenin |
| title | Cyclin G2 suppresses estrogen-mediated osteogenesis through inhibition of Wnt/β-catenin signaling |
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