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Photoactivatable senolysis with single-cell resolution reverses aging

ABSTRACT: Emerging evidence supports the use of pharmaceutical interventions to target senescent cells (SnCs) and induce their death (senolysis) to extend a healthy lifespan. The challenge then becomes how to achieve precise, broad-spectrum and tractable senolysis. To this end, we have designed a novel senotherapeutic agent with an unprecedented integrated strategy

ORGANISM(S): Mus musculus

PROVIDER: GSE213846 | GEO | 2022/09/24

REPOSITORIES: GEO

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Photoactivatable senolysis with single-cell resolution reverses aging

Project description:Cellular senescence is a crucial biological process associated with pathologies of aging. The elimination of senescent cells (SnCs) for the purpose to extend healthy lifespan has been supported by emerging evidence, which causes the exploration of drug approaches to induce SnCs death (senolysis). The challenge then becomes how to achieve the precision, broad-spectrum and controllability of senolysis. To this end, we here propose an unprecedented integration strategy to design a senotherapeutic agent

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Photoactivatable senolysis with single-cell resolution reverses aging

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Acceleration of beta cell aging plays a key role in diabetes and senolysis improves metabolic, functional and cellular outcomes

Project description:The risk of type 2 diabetes increases with age. Although changes in function and proliferation of aged beta cells resemble those preceding the development of diabetes, the contribution of beta cell aging and senescence remains unclear. The proportion of aged beta cells increases with animal age but even in young mice, senescent beta cells can be found. We showed that different models of insulin resistance accelerated aging and senescence marker expression in beta cells, BGal, led to loss of function and impaired glucose tolerance. Clearance of p16Ink4a+ cells, using the INK-ATTAC mouse model, ameliorated glucose metabolism, insulin secretion and decreased expression of aging, senescence and SASP genes in pancreatic islets. Senolytic drug ABT263 also improved glucose metabolism and beta cell identity when administered during insulin resistance. Human beta cells from diabetic and non-diabetic donors shared some of the same biology laying the foundation for translation into humans. These novel findings lay the framework to pursue senolysis of beta cells as a preventive and alleviating strategy for T2D.

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Project description:Senescent cells (SnCs) are considered the driving force of aging; therefore, restoring the normal function of SnCs or reversing the senescence-associated secretory phenotype (SASP) may have anti-aging effects. Current anti-aging strategies include destroying, or reprogramming, SnCs and inhibiting SASP. However, significant challenges persist, such as the progressive loss of tissue function and risk of tumorigenesis. Herein, we report a Senoreviver strategy that breaks cell cycle arrest and reverses SASP simultaneously via human embryonic stem cell exosome (hESC-Exo)-mediated delivery of miR-302b. miRNA-seq analysis revealed that hESC-Exos enriches miR-302 family members. Ago2 CLIP-seq mapping revealed that miR-302b could repress the cell cycle inhibitors Cdkn1a and Ccng2, which collectively restored the proliferative capacity of SnCs and reversed SASP. Our study provides a Senoreviver strategy to rejuvenate SnCs in vitro and in vivo, rather than eliminate or reprogram them, thus holding great promise for maintaining tissue homeostasis, extending the health span, and countering age-related diseases.

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Project description:Cellular senescence is a stress or damage response that causes a permanent proliferative arrest and secretion of numerous factors with potent biological activities. This senescence-associated secretory phenotype (SASP) has been characterized largely for secreted proteins that participate in embryogenesis, wound healing, inflammation and many age-related pathologies. By contrast, lipid components of the SASP are understudied. We show that senescent cells activate the biosynthesis of several oxylipins that promote segments of the SASP and reinforce the proliferative arrest. Notably, senescent cells synthesize and accumulate an unstudied intracellular prostaglandin, 1a,1b-dihomo-15-deoxy-delta-12,14-prostaglandin J2. Released 15-deoxy-delta-12,14-prostaglandin J2 is a biomarker of senolysis in culture and in vivo. This and other prostaglandin D2-related lipids promote the senescence arrest and SASP by activating RAS signaling. These data identify an important aspect of cellular senescence and a method to detect senolysis

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