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AUF-1 affected genes in human skin cells

ABSTRACT: This study aims to evaluate the effect of AUF-1 knokdown on the function and global gene expression in human skin cells. Cells with AUF1 silencing were compared with control cells by RNA-Seq. Cell senescence is a tightly controlled, programmed process. Although the mechanism of cell senescence is unclear, the concept that cell aging is an interaction results between enviomental and genetic factors has been accepted. Changes in the expression of related genes are the genetic basis of cell senescence. AUF1 gene has been proved that can recognize classical mRNA and regulated its expression level. These classical mRNA include those encoding cecle-regulating proteins, apoptotic regulators, cytokines and proto-oncogenes. Our study use overexpression and interference lentivirus of AUF1 to transfect WS1 cell to process cell transcriptome sequencing. Through the Bioinformatics analysis results, we want to see some different expressed genes related to cell cecle, cell apoptosis and so on. Our study can provide basis research to further expound AUF1 gene, play an important role of aging mechanism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE138621 | GEO | 2019/10/10

REPOSITORIES: GEO

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Project description:Introduction: At the molecular level, cellular aging involves changes in multiple gene pathways, which can produce many aging phenotypes. In the liver, senescence changes lead to impaired hepatic function. We hypothesized that the natural hepatic aging process is driven by sex-dependent mechanisms. Purpose: We studied our well-established model of aging in which we have previously determined aging of metabolism, reproduction and endocrine systems. We performed liver transcriptomics (RNA-seq) on male and female rats at 110 and 650 days (d) fed with normal rat chow to determine changes key signaling pathways related to senescence processes. Methods: To identify the functional F1 liver changes due to natural aging processes, we evaluated the differentially expressed genes (DEGs) between 650d and 110d in males and females, with separate pairwise comparisons due to the marked differences. Genes were filtered based on ?1.4 fold change (FC) and nominal P value <0.05 (Studentｴs t-test). Results: We found that the natural liver aging process shows sex-differences. RNA-seq revealed more male (3,967) than female (283) differentially expressed genes (DEG) and pathways over the 110d to 650d period studied. Cell cycle pathway signaling in males was accompanied by decreased protein and gene expression of key genes (CDK2, CDK4, Cycd and PCNA) and an increase of p57 at 650d vs. 110d. In females, protein and gene expression of cell growth regulators such as p15 and p21, that inhibit cell cycle G1 progression were increased. Moreover, additionally the cell senescence pathway showed sexual dimorphism in liver gene regulation. Conclusions: Our results demonstrate how the natural aging process affects the liver transcriptome signature in a sex-dependent manner, specifically in cell cycle and cell senescence pathways, pathways that contribute in a major fashion to the development of aging-induced liver diseases. Understanding cellular senescence pathways involved in the natural aging process will aid evaluation of mechanisms associated with altered aging and frailty trajectories.

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AUF-1 affected genes in human skin cells

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