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Photoactivatable senolysis with single-cell resolution reverses aging

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE186522 | GEO | 2021/10/27

REPOSITORIES: GEO

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Photoactivatable senolysis with single-cell resolution reverses aging

Project description: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

2022-09-24 | GSE213846 | GEO

Photoactivatable senolysis with single-cell resolution reverses aging

Project description:Photoactivatable senolysis with single-cell resolution reverses aging

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gene expression of aorta of ApoE KO mice after Gpnmb vaccine treatment

Project description:Accumulation of senescent cells in various tissues has been reported to have a pathological role in age-associated diseases. Inhibition of cellular aging signals prevents the onset of age-associated pathology, but there is a risk of promoting carcinogenesis. Elimination of senescent cells (senolysis) was recently reported to reversibly improve pathological changes related to aging in aged mice without increasing the development of cancer. Here we report that glycoprotein nonmetastatic melanoma protein B (Gpnmb) could be a molecular target for senolytic therapy. Elimination of Gpnmb-positive cells by vaccination improved atherosclerosis.

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Silver nanocolloids affects glycosylation in medaka fish to cause embryonic malformation.

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RNA sequencing analysis of ARV825 target genes in senescent cells

Project description:Although cellular senescence acts primarily as a tumor suppression mechanism, the accumulation of senescent cells in vivo eventually exerts deleterious side effects through inflammatory/tumor-promoting factor secretion. Thus, the development of new drugs that cause the specific elimination of senescent cells, termed senolysis, is anticipated. Here, by an unbiased high-throughput screening of chemical compounds and a bio-functional analysis, we identify ARV825 as a promising senolytic drug. ARV825 treatment eliminates senescent hepatic stellate cells in obese mouse livers, accompanied by the reduction of liver cancer development. Furthermore, the elimination of chemotherapy-induced senescent cells by ARV825 increases the efficacy of chemotherapy against xenograft tumors in immunocompromised mice. These results reveal the vulnerability of senescent cells and open up possibilities for its control.

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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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Transfer learning of an in vivo-derived senescence signature identifies conserved tissue-specific senescence across species and diverse pathologies [bulk RNA-seq]

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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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