miR-543 and miR-590-3p regulate human mesenchymal stem cell aging via direct targeting of AIMP3/p18

Seunghee Lee, Kyung Rok Yu, Young Sil Ryu, Young Sun Oh, In Sun Hong, Hyung Sik Kim, Jin Young Lee, Sunghoon Kim, Kwang Won Seo, Kyung Sun Kang

Research output: Contribution to journalArticlepeer-review

46 Citations (Scopus)


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.

Original languageEnglish
Article number9724
Issue number6
Publication statusPublished - 2014 Nov 21

Bibliographical note

Publisher Copyright:
© 2014, American Aging Association.

All Science Journal Classification (ASJC) codes

  • Ageing
  • Geriatrics and Gerontology


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