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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

2021-10-27 | GSE186522 | GEO

Photoactivatable senolysis with single-cell resolution reverses aging

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Photoactivatable senolysis with single-cell resolution reverses aging

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

Project description:We observed silver nanocolloids (SNCs) exposure to medaka embryo induced morphological deformities like shortened body and undeveloped head and eyes, and our gene expression analysis using medaka oligo DNA microarray suggested that glycan/glycosylation genes, such as gns and alg2, might be the targets of SNCs' toxicity. Validation studies of gns and alg2 gene expressions by qPCR showed stage-dependent and altered mRNA expression patterns, and their altered expressions were more severe in earlier stages of embryogenesis. A result from structural analysis of glycan revealed that stage 11 was the most sensitive stage to SNCs exposure, and stress seemed to be imposed upon endplasmic reticulum (ER) by SNCs. In fact, qPCR analysis of ER mannosidase demonstrated that N-glycan synthesis in ER was inhibited by SNCs. Overall, this study revealed that SNCs exposure caused embryonic malformations through disruption of glycan biosynthetic pathway in ER.

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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:Glutaminase-1 Inhibition Alleviates Senescence of Wharton’s Jelly-derived Mesenchymal Stem Cells via Senolysis.

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Suppression of LBR by miR-340 disrupts chromatin, promotes cell senescence, and enhances senolysis

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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 state of permanent growth arrest that plays an important role in wound healing, tissue fibrosis, and tumor suppression. Despite their pathological role and therapeutic interest, senescent cells’ (SnCs) phenotype in vivo remains unclear. Here, we developed an in vivo-derived senescence signature using a foreign body response (FBR) fibrosis model in a SnC reporter mouse. We identified stromal cells as the primary SnC in the FBR and produced a SnC transcriptomic signature. Transfer learning identified SnCs in diverse murine and human data single cell RNAseq (scRNAseq) sets. Further, we found both conserved and tissue-specific SnC and secretory phenotypes. Signaling analysis uncovered crosstalk between SnCs and myeloid cells via an IL34-CSF1R-TGFbR signaling axis, contributing to angiogenic and fibrotic responses. Overall, our study identifies a conserved transcriptional profile of SnCs and transfer learning approach that may be broadly applied to identify and understand senescence in vivo.

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