miR-543 and miR-590-3p regulate human mesenchymal stem cell aging via direct targeting of AIMP3/p18
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- 作者：Seunghee Lee (1) (2) (3)
Kyung-Rok Yu (1) (2)
Young-Sil Ryu (1) (2)
Young Sun Oh (4) (5)
In-Sun Hong (6) (7)
Hyung-Sik Kim (1) (2) (3)
Jin Young Lee (1) (2)
Sunghoon Kim (4) (5)
Kwang-Won Seo (1) (2) (3)
Kyung-Sun Kang (1) (2) - 关键词：AIMP3/p18 ; Stem cell ; Aging ; miR ; 543 ; miR ; 590 ; 3p
- 刊名：AGE
- 出版年：2014
- 出版时间：December 2014
- 年：2014
- 卷：36
- 期：6
- 全文大小：2,558 KB
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Kyung-Rok Yu (1) (2)
Young-Sil Ryu (1) (2)
Young Sun Oh (4) (5)
In-Sun Hong (6) (7)
Hyung-Sik Kim (1) (2) (3)
Jin Young Lee (1) (2)
Sunghoon Kim (4) (5)
Kwang-Won Seo (1) (2) (3)
Kyung-Sun Kang (1) (2)
1. Adult Stem Cell Research Center, College of Veterinary Medicine, Seoul National University, Seoul, 151-742, Republic of Korea
2. Research Institute for Veterinary Medicine, College of Veterinary Medicine, Seoul National University, Seoul, 151-742, Republic of Korea
3. Institute for Stem Cell and Regenerative Medicine in Kang Stem Biotech, Biotechnology Incubating Center, Seoul National University, Seoul, 151-742, Republic of Korea
4. Medicinal Bioconvergence Research Center, Seoul National University, Seoul, 151-742, Republic of Korea
5. WCU Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Suwon, 443-270, Republic of Korea
6. Department of Molecular Medicine, Gachon University, Incheon, Republic of Korea
7. Lee Gil Ya Cancer and Diabetes Institute, Incheon, Republic of Korea - ISSN：1574-4647
文摘
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.