Nat Commun. 2020; 11(1): 2202.
A single-cell transcriptomic landscape of primate arterial aging
Weiqi Zhang 1 2 3 4 5, Shu Zhang 6 7, Pengze Yan 3 8, Jie Ren 7 9, Moshi Song 3 5 8, Jingyi Li 2 3 8, Jinghui Lei 4, Huize Pan 2 3, Si Wang 3 5 8, Xibo Ma 3 10, Shuai Ma 2 3 8, Hongyu Li 2 3, Fei Sun 2 3, Haifeng Wan 3 5 11, Wei Li 3 5 11, Piu Chan 4, Qi Zhou 3 5 11, Guang-Hui Liu 12 13 14 15 16, Fuchou Tang 17 18 19 20, Jing Qu 21 22 23
- 1 CAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing, 100101, China.
- 2 National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
- 3 University of Chinese Academy of Sciences, Beijing, 100049, China.
- 4 Beijing Institute for Brain Disorders, Advanced Innovation Center for Human Brain Protection, and National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing, China.
- 5 Institute for Stem cell and Regeneration, CAS, Beijing, 100101, China.
- 6 College of Life Sciences, Peking University, Beijing, 100871, China.
- 7 Biomedical Institute for Pioneering Investigation via Convergence, Peking University, Beijing, 100871, China.
- 8 State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
- 9 Peking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China.
- 10 CBSR&NLPR, Institute of Automation, Chinese Academy of Sciences, Beijing, 100190, China.
- 11 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
- 12 National Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China. ghliu@ioz.ac.cn.
- 13 University of Chinese Academy of Sciences, Beijing, 100049, China. ghliu@ioz.ac.cn.
- 14 Beijing Institute for Brain Disorders, Advanced Innovation Center for Human Brain Protection, and National Clinical Research Center for Geriatric Disorders, Xuanwu Hospital Capital Medical University, Beijing, China. ghliu@ioz.ac.cn.
- 15 Institute for Stem cell and Regeneration, CAS, Beijing, 100101, China. ghliu@ioz.ac.cn.
- 16 State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China. ghliu@ioz.ac.cn.
- 17 College of Life Sciences, Peking University, Beijing, 100871, China. tangfuchou@pku.edu.cn.
- 18 Biomedical Institute for Pioneering Investigation via Convergence, Peking University, Beijing, 100871, China. tangfuchou@pku.edu.cn.
- 19 Peking-Tsinghua Center for Life Sciences, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing, 100871, China. tangfuchou@pku.edu.cn.
- 20 Ministry of Education Key Laboratory of Cell Proliferation and Differentiation, Beijing, 100871, China. tangfuchou@pku.edu.cn.
- 21 University of Chinese Academy of Sciences, Beijing, 100049, China. qujing@ioz.ac.cn.
- 22 Institute for Stem cell and Regeneration, CAS, Beijing, 100101, China. qujing@ioz.ac.cn.
- 23 State Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China. qujing@ioz.ac.cn.
Our understanding of how aging affects the cellular and molecular components of the vasculature and contributes to cardiovascular diseases is still limited. Here we report a single-cell transcriptomic survey of aortas and coronary arteries in young and old cynomolgus monkeys. Our data define the molecular signatures of specialized arteries and identify eight markers discriminating aortic and coronary vasculatures. Gene network analyses characterize transcriptional landmarks that regulate vascular senility and position FOXO3A, a longevityassociated transcription factor, as a master regulator gene that is downregulated in six subtypes of monkey vascular cells during aging. Targeted inactivation of FOXO3A in human vascular endothelial cells recapitulates the major phenotypic defects observed in aged monkey arteries, verifying FOXO3A loss as a key driver for arterial endothelial aging. Our study provides a critical resource for understanding the principles underlying primate arterial aging and contributes important clues to future treatment of age-associated vascular disorders.
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