Similar Datasets
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
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
Project description:Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest
| PRJNA1036164 | ENA
Project description:Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [scRNA-Seq]
| PRJNA1036182 | ENA
Project description:Exosomal miR-302b rejuvenates aging mice by reversing cell cycle arrest [LO2 scRNA-Seq]
| PRJNA1036180 | ENA
Project description:Periodontal disease is an age-associated disorder clinically defined by periodontal bone loss, inflammation of the specialized tissues that surround and support the tooth, and microbiome dysbiosis. Currently, there is no therapy for reversing periodontal disease, and treatment is generally restricted to preventive measures or tooth extraction. The FDA-approved drug rapamycin slows aging and extends lifespan in multiple organisms, including mice. Here, we demonstrate that short-term treatment with rapamycin rejuvenates the aged oral cavity of elderly mice, including regeneration of periodontal bone, attenuation of gingival and periodontal bone inflammation, and revertive shift of the oral microbiome toward a more youthful composition. This provides a geroscience strategy to potentially rejuvenate oral health and reverse periodontal disease in the elderly.
| S-EPMC7220376 | biostudies-literature
Project description:MicroRNAs (miRNAs) are a class of small regulatory RNAs that are thought to be involved in diverse biological processes by regulating gene expression. Numerous miRNAs have been identified in various species, and many more miRNAs remain to be detected. Generally, hundreds of mRNAs have been predicted to be potential targets of one miRNA, so it is a great challenge to identify the genuine miRNA targets. Here, we generated the cell lines depleted of Drosha protein and screened dozens of transcripts (including Cyclin D1) regulated potentially by miRNA-mediated RNA silencing pathway. On the basis of miRNA expressing library, we established a miRNA targets reverse screening method by using luciferase reporter assay. By this method, we found that the expression of Cyclin D1 (CCND1) was regulated by miR-16 family directly, and miR-16 induced G1 arrest in A549 cells partially by CCND1. Furthermore, several other cell cycle genes were revealed to be regulated by miR-16 family, including Cyclin D3 (CCND3), Cyclin E1 (CCNE1) and CDK6. Taken together, our data suggests that miR-16 family triggers an accumulation of cells in G0/G1 by silencing multiple cell cycle genes simultaneously, rather than the individual target.
| S-EPMC2532718 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2015-05-20 | E-GEOD-58155 | biostudies-arrayexpress
Project description:BackgroundFunctional decline in stem cell-mediated regeneration contributes to aging associated with cellular senescence in c-kit+ cardiac progenitor cells (CPCs). Clinical implementation of CPC-based therapy in elderly patients would benefit tremendously from understanding molecular characteristics of senescence to antagonize aging. Nucleostemin (NS) is a nucleolar protein regulating stem cell proliferation and pluripotency.ObjectivesThis study sought to demonstrate that NS preserves characteristics associated with "stemness" in CPCs and antagonizes myocardial senescence and aging.MethodsCPCs isolated from human fetal (fetal human cardiac progenitor cell [FhCPC]) and adult failing (adult human cardiac progenitor cell [AhCPC]) hearts, as well as young (young cardiac progenitor cell [YCPC]) and old mice (old cardiac progenitor cell [OCPC]), were studied for senescence characteristics and NS expression. Heterozygous knockout mice with 1 functional allele of NS (NS+/-) were used to demonstrate that NS preserves myocardial structure and function and slows characteristics of aging.ResultsNS expression is decreased in AhCPCs relative to FhCPCs, correlating with lowered proliferation potential and shortened telomere length. AhCPC characteristics resemble those of OCPCs, which have a phenotype induced by NS silencing, resulting in cell flattening, senescence, multinucleated cells, decreased S-phase progression, diminished expression of stemness markers, and up-regulation of p53 and p16. CPC senescence resulting from NS loss is partially p53 dependent and is rescued by concurrent silencing of p53. Mechanistically, NS induction correlates with Pim-1 kinase-mediated stabilization of c-Myc. Engineering OCPCs and AhCPCs to overexpress NS decreases senescent and multinucleated cells, restores morphology, and antagonizes senescence, thereby preserving phenotypic properties of "stemness." Early cardiac aging with a decline in cardiac function, an increase in senescence markers p53 and p16, telomere attrition, and accompanied CPC exhaustion is evident in NS+/- mice.ConclusionsYouthful properties and antagonism of senescence in CPCs and the myocardium are consistent with a role for NS downstream from Pim-1 signaling that enhances cardiac regeneration.
| S-EPMC4297321 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-12-23 | GSE25009 | GEO