Multiplexed single-cell imaging reveals diverging subpopulations with distinct senescence phenotypes during long-term senescence induction.

Garrett A Sessions, Madeline V Loops, Brian O Diekman, Jeremy E Purvis

Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA.Department of Cell Biology and Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA. · pubmed

Paper

Abstract

Cellular senescence is a phenotypic state that contributes to the progression of age-related disease through secretion of pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Understanding the process by which healthy cells become senescent and develop SASP factors is critical for improving the identification of senescent cells and, ultimately, understanding tissue dysfunction. Here, we reveal how the duration of cellular stress modulates the SASP in distinct subpopulations of senescent cells. We used multiplex, single-cell imaging to build a proteomic map of senescence induction in human epithelial cells induced to senescence over the course of 31 days. We map how the expression of SASP proteins increases alongside other known senescence markers such as p53, p21, and p16

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Research summary

The paper claims that the duration of cellular stress influences the senescence-associated secretory phenotype (SASP) in distinct subpopulations of senescent cells. This research is relevant as it addresses the mechanisms underlying cellular senescence, which is a key factor in aging and age-related diseases, potentially contributing to the understanding of tissue dysfunction and longevity.

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