Journal
DEVELOPMENTAL CELL
Volume 56, Issue 3, Pages 383-+Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2020.11.002
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Funding
- National Key Research and Development Program of China [2018YFC2000100, 2020YFA0804000, 2020YFA0113400, 2017YFA0103304, 2017YFA0102802, 2018YFA0107203, 2020YFE0201600]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDA16010100]
- National Natural Science Foundation of China [82001477, 81921006, 81625009, 91749202, 91949209, 91749123, 31671429, 81671377, 81701388, 81822018, 81870228, 81861168034, 81922027, 81670444, 82071588, 32000500]
- Program of the Beijing Municipal Science and TechnologyCommission [Z191100001519005]
- Beijing Natural Science Foundation [Z190019, JQ20031]
- Beijing Municipal Commission of Health and Family Planning [PXM2018_026283_000002]
- Advanced Innovation Center for Human Brain Protection [3500-1192012]
- Key Research Program of the Chinese Academy of Sciences [KFZD-SW-221]
- K.C. Wong Education Foundation [GJTD-2019-06, GJTD-2019-08]
- Youth Innovation Promotion Association of CAS [2016093]
- State Key Laboratory of Membrane Biology
- State Key Laboratory of Stem Cell and Reproductive Biology
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Single-cell RNA sequencing of human eyelid skin revealed progressive accumulation of photoaging-related changes and increased chronic inflammation with age. Transcriptional factors involved in the developmental process showed early-onset decline during aging. Inhibition of key transcription factors HES1 and KLF6 compromised cell proliferation, increased inflammation, and accelerated cellular senescence during aging.
Skin undergoes constant self-renewal, and its functional decline is a visible consequence of aging. Understanding human skin aging requires in-depth knowledge of the molecular and functional properties of various skin cell types. We performed single-cell RNA sequencing of human eyelid skin from healthy individuals across different ages and identified eleven canonical cell types, as well as six subpopulations of basal cells. Further analysis revealed progressive accumulation of photoaging-related changes and increased chronic inflammation with age. Transcriptional factors involved in the developmental process underwent early-onset decline during aging. Furthermore, inhibition of key transcription factors HES1 in fibroblasts and KLF6 in keratinocytes not only compromised cell proliferation, but also increased inflammation and cellular senescence during aging. Lastly, we found that genetic activation of HES1 or pharmacological treatment with quercetin alleviated cellular senescence of dermal fibroblasts. These findings provide a single-cell molecular framework of human skin aging, providing a rich resource for developing therapeutic strategies against aging-related skin disorders.
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