miR‐17, miR‐19b, miR‐20a, and miR‐106a are down‐regulated in human aging

摘要: Aging is a multifactorial process where deterioration of body functions driven by stochastic damage while counteracted distinct genetically encoded repair systems. To better understand the genetic component aging, many studies have addressed gene and protein expression profiles various aging model systems engaging different organisms from yeast to human. The recently identified small non-coding miRNAs are potent post-transcriptional regulators that can modify up several hundred target genes per single miRNA, similar transcription factors. Increasing evidence shows contribute regulation most if not all important physiological processes, including aging. However, so far contribution age-related senescence-related changes in remains elusive. address this question, we selected four replicative cell models endothelial cells, replicated CD8+ T renal proximal tubular epithelial skin fibroblasts. Further included were three organismal foreskin, mesenchymal stem populations old young donors. Using locked nucleic acid-based miRNA microarrays, commonly regulated miRNAs, miR-17 down-regulated seven; miR-19b miR-20a, six models; miR-106a five models. Decrease these correlated with increased transcript levels some established genes, especially cdk inhibitor p21/CDKN1A. These results establish as novel markers humans.