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Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [LO2 scRNA-Seq]

ABSTRACT: Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [LO2 scRNA-Seq]

PROVIDER: PRJNA1036180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26681307_1.fastq.gz	Fastqsanger.gz
	SRR26681307_2.fastq.gz	Fastqsanger.gz
	SRR26681308_1.fastq.gz	Fastqsanger.gz
	SRR26681308_2.fastq.gz	Fastqsanger.gz

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Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest

Project description:Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest

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Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [scRNA-Seq]

Project description:Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [scRNA-Seq]

| PRJNA1036182 | ENA

Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [scRNA-Seq]

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.

2024-11-01 | GSE247074 | GEO

Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [LO2 scRNA-Seq]

Project description:Cellular senescence is a hallmark of aging characterized by a stable exit from the cell cycle in response to cellular damage and stress. Senescent cells (SnCs) are closely associated with aging and aging-related disorders, making them a potential target for slowing aging. In this study, we developed a tool for dynamically monitoring the p21 signaling to determine the degree of cellular senescence, named p21-YFP LO2. The senescent cells were prepared by FCM sorting targeting p21-YFP LO2 treated with 50 nM Dox for 48 h based on the YFP signaling. The single-cell RNA sequencing (scRN-seq) analysis was performed to observe the effects of human embryonic stem cell-derived exosomes (hESC-Exos) on the transcriptional profiles of SnCs. We specifically demonstrated that hESC-Exos enable SnCs to reverse the cell cycle arrest and restore their proliferative capacity in vitro.

2024-11-01 | GSE247073 | GEO

Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-11-01 | GSE247076 | GEO

Caloric restriction rejuvenates myofiber growth in heart failure

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MicroRNA expression during cell cycle arrest

Project description:The miR-16 family, which targets genes important for the G1-S transition, is a known modulator of the cell cycle, and members of this family are often deleted or down-regulated in many types of cancers. Here we report the reciprocal relationship - that of the cell cycle controlling the miR-16 family. Levels of this family increase rapidly as cells are arrested in G0. Conversely, as cells are released from G0 arrest, levels of the miR-16 family rapidly decrease. Such rapid changes are made possible by the unusual instabilities of several family members. The repression mediated by the miR-16 family is sensitive to these cell cycle changes, which suggests that the rapid up-regulation of the miR-16 family reinforces cell cycle arrest in G0. Upon cell cycle re-entry, the rapid decay of several members allows levels of the family to decrease, alleviating repression of target genes and allowing proper resumption of the cell cycle. Small RNAs were profiled by high-throughput sequencing either during synchronous release after serum starvation or during cell-cycle arrest by contact inhibition.

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MicroRNA expression during cell cycle arrest

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