Sirt3-MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts
Increasing evidence has suggested an important role played by reactive oxygen species in the patho- genesis of osteoporosis. Tobacco smoking is an important risk factor for the development of osteo- porosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nico...
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| Veröffentlicht in: | Acta biochimica et biophysica Sinica 2015-04, Vol.47 (4), p.306-312 |
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| container_title | Acta biochimica et biophysica Sinica |
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| creator | Li, Yong Yu, Chen Shen, Guangsi Li, Guangfei Shen, Junkang Xu, Youjia Gong, Jianping |
| description | Increasing evidence has suggested an important role played by reactive oxygen species in the patho- genesis of osteoporosis. Tobacco smoking is an important risk factor for the development of osteo- porosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nicotine promotes osteoporosis is not fully understood. Here, in this study, we found that nicotine- induced mitochondrial oxidative stress and mitochondrial DNA （mtDNA） damage in osteoblasts dif- ferentiated from mouse mesenchymal stem cell. The activity of MnSOD, one of the mitochondrial anti-oxidative enzymes, was significantly reduced by nicotine due to the reduced level of Sirt3. More- over, it was also found that Sirt3 could promote MnSOD activity by deacetylating MnSOD. Finally, Mn（Ⅲ）tetrakis （4-benzoic acid） porphyrin （MnTBAP, a MnSOD mimetic） was found to markedly re- duce the effect of nicotine on osteoblasts. In summary, Sirt3-MnSOD axis was identified as a nega- tive component in nicotine-induced rnitochondrial oxidative stress and mtDNA damage, and MnTBAP may serve as a potential therapeutic drug for osteoporosis. |
| doi_str_mv | 10.1093/abbs/gmv013 |
| format | Article |
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Tobacco smoking is an important risk factor for the development of osteo- porosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nicotine promotes osteoporosis is not fully understood. Here, in this study, we found that nicotine- induced mitochondrial oxidative stress and mitochondrial DNA （mtDNA） damage in osteoblasts dif- ferentiated from mouse mesenchymal stem cell. The activity of MnSOD, one of the mitochondrial anti-oxidative enzymes, was significantly reduced by nicotine due to the reduced level of Sirt3. More- over, it was also found that Sirt3 could promote MnSOD activity by deacetylating MnSOD. Finally, Mn（Ⅲ）tetrakis （4-benzoic acid） porphyrin （MnTBAP, a MnSOD mimetic） was found to markedly re- duce the effect of nicotine on osteoblasts. In summary, Sirt3-MnSOD axis was identified as a nega- tive component in nicotine-induced rnitochondrial oxidative stress and mtDNA damage, and MnTBAP may serve as a potential therapeutic drug for osteoporosis.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.1093/abbs/gmv013</identifier><identifier>PMID: 25757953</identifier><language>eng</language><publisher>China</publisher><subject>Acetylation - drug effects ; Animals ; Blotting, Western ; Cells, Cultured ; DNA Damage ; DNA, Mitochondrial - genetics ; Down-Regulation - drug effects ; Ganglionic Stimulants - toxicity ; Humans ; Metalloporphyrins - pharmacology ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria - drug effects ; Mitochondria - genetics ; Mitochondria - metabolism ; MnSOD ; Nicotine - toxicity ; Osteoclasts - cytology ; Osteoclasts - drug effects ; Osteoclasts - metabolism ; Oxidative Stress - drug effects ; Reactive Oxygen Species - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sirtuin 3 - genetics ; Sirtuin 3 - metabolism ; Superoxide Dismutase - metabolism ; 尼古丁 ; 成骨细胞分化 ; 损伤 ; 氧化应激 ; 线粒体DNA ; 诱导 ; 锰超氧化物歧化酶</subject><ispartof>Acta biochimica et biophysica Sinica, 2015-04, Vol.47 (4), p.306-312</ispartof><rights>The Author 2015. 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Tobacco smoking is an important risk factor for the development of osteo- porosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nicotine promotes osteoporosis is not fully understood. Here, in this study, we found that nicotine- induced mitochondrial oxidative stress and mitochondrial DNA （mtDNA） damage in osteoblasts dif- ferentiated from mouse mesenchymal stem cell. The activity of MnSOD, one of the mitochondrial anti-oxidative enzymes, was significantly reduced by nicotine due to the reduced level of Sirt3. More- over, it was also found that Sirt3 could promote MnSOD activity by deacetylating MnSOD. Finally, Mn（Ⅲ）tetrakis （4-benzoic acid） porphyrin （MnTBAP, a MnSOD mimetic） was found to markedly re- duce the effect of nicotine on osteoblasts. In summary, Sirt3-MnSOD axis was identified as a nega- tive component in nicotine-induced rnitochondrial oxidative stress and mtDNA damage, and MnTBAP may serve as a potential therapeutic drug for osteoporosis.</description><subject>Acetylation - drug effects</subject><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cells, Cultured</subject><subject>DNA Damage</subject><subject>DNA, Mitochondrial - genetics</subject><subject>Down-Regulation - drug effects</subject><subject>Ganglionic Stimulants - toxicity</subject><subject>Humans</subject><subject>Metalloporphyrins - pharmacology</subject><subject>Mice, 129 Strain</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - genetics</subject><subject>Mitochondria - metabolism</subject><subject>MnSOD</subject><subject>Nicotine - toxicity</subject><subject>Osteoclasts - cytology</subject><subject>Osteoclasts - drug effects</subject><subject>Osteoclasts - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Sirtuin 3 - genetics</subject><subject>Sirtuin 3 - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><subject>尼古丁</subject><subject>成骨细胞分化</subject><subject>损伤</subject><subject>氧化应激</subject><subject>线粒体DNA</subject><subject>诱导</subject><subject>锰超氧化物歧化酶</subject><issn>1672-9145</issn><issn>1745-7270</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c9PFDEUB_DGSATRk3fTeCIxA-301_RIQNEE5ICeJ2_aN2vJTLu0XYL_PbPZhaun18On37y8LyGfODvlzIozGIZytpofGRdvyBE3UjWmNezt8tambSyX6pC8L-WeMaE1Z-_IYauMMlaJI3J_F3IVzU28u72k8BQKzbjOWAoWGoNLNURsQvQbh57OoSb3N0WfA0w0PQUPNTwiLXX7g0JcSL38dU49zLBCGiJNpWIaJii1fCAHI0wFP-7nMfnz_dvvix_N9e3Vz4vz68YJaWvj3IBmAM8NKglKCXBeOsZgtF6C8Rw7GJWSg2wFalCdFV50Gq0fvbUaxDE52eWuc3rYYKn9HIrDaYKIaVN63nFuWWds-3-qtVmWaqVY6NcddTmVknHs1znMkP_1nPXbHvptD_2uh0V_3gdvhhn9q305_AK-7OOWe64eQly9Gq2VZNYIIZ4BJT2SAw</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>Li, Yong</creator><creator>Yu, Chen</creator><creator>Shen, Guangsi</creator><creator>Li, Guangfei</creator><creator>Shen, Junkang</creator><creator>Xu, Youjia</creator><creator>Gong, Jianping</creator><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</scope><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>7X8</scope><scope>7QP</scope><scope>7TM</scope></search><sort><creationdate>20150401</creationdate><title>Sirt3-MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts</title><author>Li, Yong ; Yu, Chen ; Shen, Guangsi ; Li, Guangfei ; Shen, Junkang ; Xu, Youjia ; Gong, Jianping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c349t-ccbe7bad17e54a553acd4c00af9d4a7d1e8af554b423e6a5893d386e9dfd996a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Acetylation - drug effects</topic><topic>Animals</topic><topic>Blotting, Western</topic><topic>Cells, Cultured</topic><topic>DNA Damage</topic><topic>DNA, Mitochondrial - genetics</topic><topic>Down-Regulation - drug effects</topic><topic>Ganglionic Stimulants - toxicity</topic><topic>Humans</topic><topic>Metalloporphyrins - pharmacology</topic><topic>Mice, 129 Strain</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - genetics</topic><topic>Mitochondria - metabolism</topic><topic>MnSOD</topic><topic>Nicotine - toxicity</topic><topic>Osteoclasts - cytology</topic><topic>Osteoclasts - drug effects</topic><topic>Osteoclasts - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sirtuin 3 - genetics</topic><topic>Sirtuin 3 - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><topic>尼古丁</topic><topic>成骨细胞分化</topic><topic>损伤</topic><topic>氧化应激</topic><topic>线粒体DNA</topic><topic>诱导</topic><topic>锰超氧化物歧化酶</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Yong</creatorcontrib><creatorcontrib>Yu, Chen</creatorcontrib><creatorcontrib>Shen, Guangsi</creatorcontrib><creatorcontrib>Li, Guangfei</creatorcontrib><creatorcontrib>Shen, Junkang</creatorcontrib><creatorcontrib>Xu, Youjia</creatorcontrib><creatorcontrib>Gong, Jianping</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-自然科学</collection><collection>中文科技期刊数据库-自然科学-生物科学</collection><collection>中文科技期刊数据库- 镜像站点</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Acta biochimica et biophysica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Yong</au><au>Yu, Chen</au><au>Shen, Guangsi</au><au>Li, Guangfei</au><au>Shen, Junkang</au><au>Xu, Youjia</au><au>Gong, Jianping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sirt3-MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts</atitle><jtitle>Acta biochimica et biophysica Sinica</jtitle><addtitle>Acta Biochimica et Biophysica Sinica</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>47</volume><issue>4</issue><spage>306</spage><epage>312</epage><pages>306-312</pages><issn>1672-9145</issn><eissn>1745-7270</eissn><abstract>Increasing evidence has suggested an important role played by reactive oxygen species in the patho- genesis of osteoporosis. Tobacco smoking is an important risk factor for the development of osteo- porosis, and nicotine is one of the major components in tobacco. However, the mechanism by which nicotine promotes osteoporosis is not fully understood. Here, in this study, we found that nicotine- induced mitochondrial oxidative stress and mitochondrial DNA （mtDNA） damage in osteoblasts dif- ferentiated from mouse mesenchymal stem cell. The activity of MnSOD, one of the mitochondrial anti-oxidative enzymes, was significantly reduced by nicotine due to the reduced level of Sirt3. More- over, it was also found that Sirt3 could promote MnSOD activity by deacetylating MnSOD. Finally, Mn（Ⅲ）tetrakis （4-benzoic acid） porphyrin （MnTBAP, a MnSOD mimetic） was found to markedly re- duce the effect of nicotine on osteoblasts. In summary, Sirt3-MnSOD axis was identified as a nega- tive component in nicotine-induced rnitochondrial oxidative stress and mtDNA damage, and MnTBAP may serve as a potential therapeutic drug for osteoporosis.</abstract><cop>China</cop><pmid>25757953</pmid><doi>10.1093/abbs/gmv013</doi><tpages>7</tpages></addata></record> |
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| identifier | ISSN: 1672-9145 |
| ispartof | Acta biochimica et biophysica Sinica, 2015-04, Vol.47 (4), p.306-312 |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Acetylation - drug effects Animals Blotting, Western Cells, Cultured DNA Damage DNA, Mitochondrial - genetics Down-Regulation - drug effects Ganglionic Stimulants - toxicity Humans Metalloporphyrins - pharmacology Mice, 129 Strain Mice, Inbred C57BL Mice, Knockout Mitochondria - drug effects Mitochondria - genetics Mitochondria - metabolism MnSOD Nicotine - toxicity Osteoclasts - cytology Osteoclasts - drug effects Osteoclasts - metabolism Oxidative Stress - drug effects Reactive Oxygen Species - metabolism Reverse Transcriptase Polymerase Chain Reaction Sirtuin 3 - genetics Sirtuin 3 - metabolism Superoxide Dismutase - metabolism 尼古丁 成骨细胞分化 损伤 氧化应激 线粒体DNA 诱导 锰超氧化物歧化酶 |
| title | Sirt3-MnSOD axis represses nicotine-induced mitochondrial oxidative stress and mtDNA damage in osteoblasts |
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