1.A widely adaptable approach to generate integration-free iPSCs from non-invasively acquired human somatic cells.
Zhichao DING ; Lina SUI ; Ruotong REN ; Yanjun LIU ; Xiuling XU ; Lina FU ; Ruijun BAI ; Tingting YUAN ; Ying HAO ; Weiqi ZHANG ; Huize PAN ; Wensu LIU ; Han YU ; Concepcion Rodriguez ESTEBAN ; Xiaobing YU ; Ze YANG ; Jian LI ; Xiaomin WANG ; Juan Carlos IZPISUA BELMONTE ; Guang-Hui LIU ; Fei YI ; Jing QU
Protein & Cell 2015;6(5):386-389
Adolescent
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Adult
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Aged
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Aged, 80 and over
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Cell Culture Techniques
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methods
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Child
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Female
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Humans
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Induced Pluripotent Stem Cells
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cytology
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metabolism
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Male
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Middle Aged
3.CRISPR/Cas9 and TALE: beyond cut and paste.
Liping DENG ; Ruotong REN ; Jun WU ; Keiichiro SUZUKI ; Juan Carlos IZPISUA BELMOTE ; Guang-Hui LIU
Protein & Cell 2015;6(3):157-159
Nuclease-based genome editing has proven to be a powerful and promising tool for disease modeling and gene therapy. Recent advances in CRISPR/Cas and TALE indicate that they could also be used as a targeted regulator of gene expression, as well as being utilized for illuminating specific chromosomal structures or genomic regions.
CRISPR-Cas Systems
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genetics
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Deoxyribonucleases
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genetics
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Gene Expression Regulation
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Genetic Engineering
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Genomics
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methods
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Humans
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RNA Editing
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genetics
4.Modeling xeroderma pigmentosum associated neurological pathologies with patients-derived iPSCs.
Lina FU ; Xiuling XU ; Ruotong REN ; Jun WU ; Weiqi ZHANG ; Jiping YANG ; Xiaoqing REN ; Si WANG ; Yang ZHAO ; Liang SUN ; Yang YU ; Zhaoxia WANG ; Ze YANG ; Yun YUAN ; Jie QIAO ; Juan Carlos IZPISUA BELMONTE ; Jing QU ; Guang-Hui LIU
Protein & Cell 2016;7(3):210-221
Xeroderma pigmentosum (XP) is a group of genetic disorders caused by mutations of XP-associated genes, resulting in impairment of DNA repair. XP patients frequently exhibit neurological degeneration, but the underlying mechanism is unknown, in part due to lack of proper disease models. Here, we generated patient-specific induced pluripotent stem cells (iPSCs) harboring mutations in five different XP genes including XPA, XPB, XPC, XPG, and XPV. These iPSCs were further differentiated to neural cells, and their susceptibility to DNA damage stress was investigated. Mutation of XPA in either neural stem cells (NSCs) or neurons resulted in severe DNA damage repair defects, and these neural cells with mutant XPA were hyper-sensitive to DNA damage-induced apoptosis. Thus, XP-mutant neural cells represent valuable tools to clarify the molecular mechanisms of neurological abnormalities in the XP patients.
DNA Damage
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DNA Repair
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DNA-Binding Proteins
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genetics
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metabolism
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Female
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Humans
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Induced Pluripotent Stem Cells
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metabolism
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pathology
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Male
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Models, Biological
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Mutation
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Neural Stem Cells
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metabolism
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pathology
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Xeroderma Pigmentosum
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genetics
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metabolism
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pathology
5.Chemical screen identifies a geroprotective role of quercetin in premature aging.
Lingling GENG ; Zunpeng LIU ; Weiqi ZHANG ; Wei LI ; Zeming WU ; Wei WANG ; Ruotong REN ; Yao SU ; Peichang WANG ; Liang SUN ; Zhenyu JU ; Piu CHAN ; Moshi SONG ; Jing QU ; Guang-Hui LIU
Protein & Cell 2019;10(6):417-435
Aging increases the risk of various diseases. The main goal of aging research is to find therapies that attenuate aging and alleviate aging-related diseases. In this study, we screened a natural product library for geroprotective compounds using Werner syndrome (WS) human mesenchymal stem cells (hMSCs), a premature aging model that we recently established. Ten candidate compounds were identified and quercetin was investigated in detail due to its leading effects. Mechanistic studies revealed that quercetin alleviated senescence via the enhancement of cell proliferation and restoration of heterochromatin architecture in WS hMSCs. RNA-sequencing analysis revealed the transcriptional commonalities and differences in the geroprotective effects by quercetin and Vitamin C. Besides WS hMSCs, quercetin also attenuated cellular senescence in Hutchinson-Gilford progeria syndrome (HGPS) and physiological-aging hMSCs. Taken together, our study identifies quercetin as a geroprotective agent against accelerated and natural aging in hMSCs, providing a potential therapeutic intervention for treating age-associated disorders.
6.Deciphering primate retinal aging at single-cell resolution.
Si WANG ; Yuxuan ZHENG ; Qingqing LI ; Xiaojuan HE ; Ruotong REN ; Weiqi ZHANG ; Moshi SONG ; Huifang HU ; Feifei LIU ; Guoqiang SUN ; Shuhui SUN ; Zunpeng LIU ; Yang YU ; Piu CHAN ; Guo-Guang ZHAO ; Qi ZHOU ; Guang-Hui LIU ; Fuchou TANG ; Jing QU
Protein & Cell 2021;12(11):889-898