miR-543 and miR-590-3p regulate human mesenchymal stem cell aging via direct targeting of AIMP3/p18
- Authors
- Lee, Seunghee; Yu, Kyung-Rok; Ryu, Young-Sil; Oh, Young Sun; Hong, In-Sun; Kim, Hyung-Sik; Lee, Jin Young; Kim, Sunghoon; Seo, Kwang-Won; Kang, Kyung-Sun
- Issue Date
- Dec-2014
- Publisher
- SPRINGER
- Keywords
- AIMP3/p18; Stemcell; Aging; miR-543; miR-590-3p
- Citation
- AGE, v.36, no.6
- Journal Title
- AGE
- Volume
- 36
- Number
- 6
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12058
- DOI
- 10.1007/s11357-014-9724-2
- ISSN
- 0161-9152
- Abstract
- Previously, AIMP3 (aminoacyl-tRNAsynthetase- interacting multifunctional protein-3) was shown to be involved in the macromolecular tRNA synthetase complex or to act as a tumor suppressor. In this study, we report a novel role of AIMP3/p18 in the cellular aging of human mesenchymal stem cells (hMSCs). We found that AIMP3/p18 expression significantly increased in senescent hMSCs and in aged mouse bone marrow-derived MSCs (mBM-MSCs). AIMP3/p18 overexpression is sufficient to induce the cellular senescence phenotypes with compromised clonogenicity and adipogenic differentiation potential. To identify the upstream regulators of AIMP3/p18 during senescence, we screened for potential epigenetic regulators and for miRNAs. We found that the levels of miR-543 and miR-590-3p significantly decreased under senescence-inducing conditions, whereas the AIMP3/p18 protein levels increased. We demonstrate for the first time that miR-543 and miR-590-3p are able to decrease AIMP3/p18 expression levels through direct binding to the AIMP/p18 transcripts, which further compromised the induction of the senescence phenotype. Taken together, our data demonstrate that AIMP3/p18 regulates cellular aging in hMSCs possibly through miR-543 and miR-590-3p.
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