KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization
Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorga...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Biao Huang [verfasserIn] Bin Wang [verfasserIn] Wayne Yuk-Wai Lee [verfasserIn] Kin Pong U [verfasserIn] Kam Tong Leung [verfasserIn] Xican Li [verfasserIn] Zhenqing Liu [verfasserIn] Rui Chen [verfasserIn] Jia cheng Lin [verfasserIn] Lai Ling Tsang [verfasserIn] Baohua Liu [verfasserIn] Ye chun Ruan [verfasserIn] Hsiao Chang Chan [verfasserIn] Gang Li [verfasserIn] Xiaohua Jiang [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Übergeordnetes Werk: |
In: iScience - Elsevier, 2019, 21(2019), Seite 375-390 |
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| Übergeordnetes Werk: |
volume:21 ; year:2019 ; pages:375-390 |
| Links: |
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| DOI / URN: |
10.1016/j.isci.2019.10.041 |
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DOAJ001391984 |
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| 520 | |a Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research | ||
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10.1016/j.isci.2019.10.041 doi (DE-627)DOAJ001391984 (DE-599)DOAJbd0253eb567e4c14a2e4be4b3ba4d30d DE-627 ger DE-627 rakwb eng Biao Huang verfasserin aut KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research Science Q Bin Wang verfasserin aut Wayne Yuk-Wai Lee verfasserin aut Kin Pong U verfasserin aut Kam Tong Leung verfasserin aut Xican Li verfasserin aut Zhenqing Liu verfasserin aut Rui Chen verfasserin aut Jia cheng Lin verfasserin aut Lai Ling Tsang verfasserin aut Baohua Liu verfasserin aut Ye chun Ruan verfasserin aut Hsiao Chang Chan verfasserin aut Gang Li verfasserin aut Xiaohua Jiang verfasserin aut In iScience Elsevier, 2019 21(2019), Seite 375-390 (DE-627)1019532106 25890042 nnns volume:21 year:2019 pages:375-390 https://doi.org/10.1016/j.isci.2019.10.041 kostenfrei https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004219304213 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 21 2019 375-390 |
| spelling |
10.1016/j.isci.2019.10.041 doi (DE-627)DOAJ001391984 (DE-599)DOAJbd0253eb567e4c14a2e4be4b3ba4d30d DE-627 ger DE-627 rakwb eng Biao Huang verfasserin aut KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research Science Q Bin Wang verfasserin aut Wayne Yuk-Wai Lee verfasserin aut Kin Pong U verfasserin aut Kam Tong Leung verfasserin aut Xican Li verfasserin aut Zhenqing Liu verfasserin aut Rui Chen verfasserin aut Jia cheng Lin verfasserin aut Lai Ling Tsang verfasserin aut Baohua Liu verfasserin aut Ye chun Ruan verfasserin aut Hsiao Chang Chan verfasserin aut Gang Li verfasserin aut Xiaohua Jiang verfasserin aut In iScience Elsevier, 2019 21(2019), Seite 375-390 (DE-627)1019532106 25890042 nnns volume:21 year:2019 pages:375-390 https://doi.org/10.1016/j.isci.2019.10.041 kostenfrei https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004219304213 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 21 2019 375-390 |
| allfields_unstemmed |
10.1016/j.isci.2019.10.041 doi (DE-627)DOAJ001391984 (DE-599)DOAJbd0253eb567e4c14a2e4be4b3ba4d30d DE-627 ger DE-627 rakwb eng Biao Huang verfasserin aut KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research Science Q Bin Wang verfasserin aut Wayne Yuk-Wai Lee verfasserin aut Kin Pong U verfasserin aut Kam Tong Leung verfasserin aut Xican Li verfasserin aut Zhenqing Liu verfasserin aut Rui Chen verfasserin aut Jia cheng Lin verfasserin aut Lai Ling Tsang verfasserin aut Baohua Liu verfasserin aut Ye chun Ruan verfasserin aut Hsiao Chang Chan verfasserin aut Gang Li verfasserin aut Xiaohua Jiang verfasserin aut In iScience Elsevier, 2019 21(2019), Seite 375-390 (DE-627)1019532106 25890042 nnns volume:21 year:2019 pages:375-390 https://doi.org/10.1016/j.isci.2019.10.041 kostenfrei https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004219304213 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 21 2019 375-390 |
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10.1016/j.isci.2019.10.041 doi (DE-627)DOAJ001391984 (DE-599)DOAJbd0253eb567e4c14a2e4be4b3ba4d30d DE-627 ger DE-627 rakwb eng Biao Huang verfasserin aut KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research Science Q Bin Wang verfasserin aut Wayne Yuk-Wai Lee verfasserin aut Kin Pong U verfasserin aut Kam Tong Leung verfasserin aut Xican Li verfasserin aut Zhenqing Liu verfasserin aut Rui Chen verfasserin aut Jia cheng Lin verfasserin aut Lai Ling Tsang verfasserin aut Baohua Liu verfasserin aut Ye chun Ruan verfasserin aut Hsiao Chang Chan verfasserin aut Gang Li verfasserin aut Xiaohua Jiang verfasserin aut In iScience Elsevier, 2019 21(2019), Seite 375-390 (DE-627)1019532106 25890042 nnns volume:21 year:2019 pages:375-390 https://doi.org/10.1016/j.isci.2019.10.041 kostenfrei https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004219304213 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 21 2019 375-390 |
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10.1016/j.isci.2019.10.041 doi (DE-627)DOAJ001391984 (DE-599)DOAJbd0253eb567e4c14a2e4be4b3ba4d30d DE-627 ger DE-627 rakwb eng Biao Huang verfasserin aut KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research Science Q Bin Wang verfasserin aut Wayne Yuk-Wai Lee verfasserin aut Kin Pong U verfasserin aut Kam Tong Leung verfasserin aut Xican Li verfasserin aut Zhenqing Liu verfasserin aut Rui Chen verfasserin aut Jia cheng Lin verfasserin aut Lai Ling Tsang verfasserin aut Baohua Liu verfasserin aut Ye chun Ruan verfasserin aut Hsiao Chang Chan verfasserin aut Gang Li verfasserin aut Xiaohua Jiang verfasserin aut In iScience Elsevier, 2019 21(2019), Seite 375-390 (DE-627)1019532106 25890042 nnns volume:21 year:2019 pages:375-390 https://doi.org/10.1016/j.isci.2019.10.041 kostenfrei https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d kostenfrei http://www.sciencedirect.com/science/article/pii/S2589004219304213 kostenfrei https://doaj.org/toc/2589-0042 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2110 GBV_ILN_2112 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 21 2019 375-390 |
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KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization |
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KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization |
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KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization |
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kdm3a and kdm4c regulate mesenchymal stromal cell senescence and bone aging via condensin-mediated heterochromatin reorganization |
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KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization |
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Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research |
| abstractGer |
Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research |
| abstract_unstemmed |
Summary: Epigenomic changes and stem cell deterioration are two hallmarks of aging. Accumulating evidence suggest that senescence of mesenchymal stromal cells (MSCs) perpetuates aging or age-related diseases. Here we report that two H3K9 demethylases, KDM3A and KDM4C, regulate heterochromatin reorganization via transcriptionally activating condensin components NCAPD2 and NCAPG2 during MSC senescence. Suppression of KDM3A or KDM4C by either genetic or biochemical approach leads to robust DNA damage response and aggravates cellular senescence, whereas overexpression of KDM3A/KDM4C or NCAPD2 promotes heterochromatin reorganization and blunts DNA damage response. Moreover, MSCs derived from Kdm3a−/− mice exhibit defective chromosome organization and exacerbated DNA damage response, which are associated with accelerated bone aging. Consistently, analysis of human bone marrow MSCs and transcriptome database reveals inverse correlation of KDM3A/KDM4C and/or NCAPD2/NCAPG2 with aging. Taken together, the present finding unveils that H3K9 demethylases function as a surveillance mechanism to restrain DNA damage accumulation in stem cells during aging. : Molecular Mechanism of Gene Regulation; Cell Biology; Stem Cells Research Keywords: mesenchymal stromal cells, condensin, histone demethylase, DNA damage, bone aging, epigenetic regulation, Subject Areas: Molecular Mechanism of Gene Regulation, Cell Biology, Stem Cells Research |
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KDM3A and KDM4C Regulate Mesenchymal Stromal Cell Senescence and Bone Aging via Condensin-mediated Heterochromatin Reorganization |
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https://doi.org/10.1016/j.isci.2019.10.041 https://doaj.org/article/bd0253eb567e4c14a2e4be4b3ba4d30d http://www.sciencedirect.com/science/article/pii/S2589004219304213 https://doaj.org/toc/2589-0042 |
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