RB Maintains Quiescence and Prevents Premature Senescence through Upregulation of DNMT1 in Mesenchymal Stromal Cells》.pdf

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RB Maintains Quiescence and Prevents Premature Senescence through Upregulation of DNMT1 in Mesenchymal Stromal Cells》.pdf

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Stem Cell Reports Article RB Maintains Quiescence and Prevents Premature Senescence through Upregulation of DNMT1 in Mesenchymal Stromal Cells Shih-Pei Lin,1,10 Fang-Yao Chiu,5,10 Yu Wang,2,6 Men-Luh Yen,8 Shou-Yen Kao,2,6,* and Shih-Chieh Hung1,3,4,5,7,9,* 1Institute of Clinical Medicine 2Department of Dentistry Sciences 3Institute of Pharmacology 4Institute of Traditional Medicine, Faculty of Medicine National Yang-Ming University, Taipei 112, Taiwan, ROC 5Department of Orthopaedics and Traumatology 6Department of Stomatology 7Stem Cell Laboratory, Department of Medical Research and Education Taipei Veterans General Hospital, Taipei 112, Taiwan, ROC 8Departments of Primary Care Medicine and Obstetrics/Gynecology, National Taiwan University Hospital and College of Medicine, National Taiwan University, Taipei 100, Taiwan, ROC 9Institute of Biomedical Sciences, Academia Sinica, Taipei 105, Taiwan, ROC 10Co-ﬁrst author *Correspondence: sykao@.tw (S.-Y.K.), hungsc@.tw (S.-C.H.) /10.1016/j.stemcr.2014.10.002 This is an open access article under the CC BY-NC-ND license (/licenses/by-nc-nd/3.0/). SUMMARY Many cell therapies currently being tested are based on mesenchymal stromal cells (MSCs). However, MSCs start to enter the senescent state upon long-term expansion. The role of retinoblastoma (RB) protein in regulating MSC properties is not well studied. Here, we show that RB levels are higher in early-passage MSCs compared with late-passage MSCs. RB knockdown induces premature senescence and reduced differentiation potentials in early-passage MSCs. RB overexpression inhibits senescence and increases differentiation potentials in late-passage MSCs. Expression of DNMT1, but not DNMT3A or DNMT3B, is also higher in early-passage MSCs than in late-passage MSCs. Furthermore, DNMT1 knockdown in early-passage MSCs induces senescence and reduces differentiation potentials, whereas DNMT1 overexpression in late-passage MSCs has the