[No authors listed]
Cellular senescence is an irreversible growth arrest of cells that maintain their metabolic activities. Premature senescence can be induced by different stress factors and occurs in mouse embryonic fibroblasts (MEFs) derived from Zmpste24 metalloproteinaseâdeficient mice, a progeria mouse model of HutchinsonâGilford Progeria Syndrome. Previous studies have shown that miRâ342â5p, an intronic microRNA (miRNA/miR) reportedly involved in ageing associated diseases, is downregulated in Zmpste24â/â MEFs. However, whether miRâ342â5p is associated with the premature senescence phenotype of Zmpste24â/â MEFs remains unclear. Thus, the present study investigated the effects of miRâ342â5p on cellular senescence and cell proliferation in Zmpste24â/â MEFs. The results showed that miRâ342â5p overexpression ameliorated the cellular senescence phenotype to a certain extent, promoted cell proliferation and increased the G2+M cell cycle phase in Zmpste24â/â MEFs. Nonetheless, it was difficult to observe the opposite cell phenotypes in wildâtype (WT) MEFs transfected with the miRâ342â5p inhibitor. Growthâarrestâspecific 2 (GAS2) was identified as a target gene of miRâ342â5p in Zmpste24â/â MEFs. In addition, miRâ342â5p was identified to be downregulated in WT MEFs during replicative senescence, while Gas2 was upregulated. Taken together, these findings suggest that downregulated miRâ342â5p is involved in regulating cell proliferation and cell cycles in Zmpste24â/â MEFs by suppressing GAS2 in vitro.
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