The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter miR-21 in estrogen deficiency–induced osteoporosis
Open accessAbstract
Inflammatory cytokines, especially tumor necrosis factor α (TNF-α), have been shown to inhibit osteogenic differentiation of mesenchymal stem cells (MSCs) and bone formation in estrogen deficiency–induced osteoporosis, but the mechanism responsible remains poorly understood. MicroRNAs (miRNAs) have been shown to regulate MSC differentiation. Here, we identified a novel mechanism whereby TNF-α, suppressing the functional axis of a key miRNA (miR-21) contributes to estrogen deficiency–induced osteoporosis. In this study, we screened differentially expressed miRNAs in MSCs derived from estrogen deficiency-induced osteoporosis and found miR-21 was significantly downregulated. miR-21 was suppressed by TNF-α during the osteogenesis of MSCs. Furthermore, miR-21 was confirmed to promote the osteoblast differentiation of MSCs by repressing Spry1, which can negatively regulate the osteogenic differentiation of MSCs. Upregulating miR-21 partially rescued TNF-α–impaired osteogenesis of MSCs. Blocking TNF-α ameliorated the inflammatory environment and significantly enhanced bone formation with increased miR-21 expression and suppressed Spry1 expression in ovariectomized (OVX) mice. Our results revealed a novel function for miR-21 and suggested that suppressed miR-21 may contribute to impaired bone formation by elevated TNF-α in estrogen deficiency–induced osteoporosis. This study may indicate a molecular basis for novel therapeutic strategies against osteoporosis and other inflammatory bone diseases. © 2013 American Society for Bone and Mineral Research.
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Citations
Cites
Pathogenesis of osteoporosis: concepts, conflicts, and prospects
Raisz, L. G. (2005) · Journal of Clinical Investigation · doi:10.1172/jci27071 · Cited by 1,779 · cited 1×
“Attenuated bone formation is a key mechanism in the pathology of postmenopausal osteoporosis.((9,12,31,32)) In this study, we identify a novel mechanism in which TNF-a inhibits osteoblastic bone formation by downregulating a key miRNA (miR-21) in an osteoporosis animal model.”
BackgroundHayashita, Y., Osada, H., Tatematsu, Y., Yamada, H., Yanagisawa, K., Tomida, S., Yatabe, Y., Kawahara, K., Sekido, Y., & Takahashi, T. (2005) · Cancer Research · doi:10.1158/0008-5472.can-05-2352 · Cited by 1,511
Embryonic Stem Cell-Specific MicroRNAs
Houbaviy, H. B., Murray, M. F., & Sharp, P. A. (2003) · Developmental Cell · doi:10.1016/s1534-5807(03)00227-2 · Cited by 1,129
Estrogen deficiency and bone loss: an inflammatory tale
Weitzmann, M. N. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28550 · Cited by 990
miR‐21: a small multi‐faceted RNA
Krichevsky, A. M., & Gabriely, G. (2009) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2008.00556.x · Cited by 987
Changes in Proinflammatory Cytokine Activity after Menopause
Pfeilschifter, J., Köditz, R., Pfohl, M., & Schatz, H. (2002) · Endocrine Reviews · doi:10.1210/edrv.23.1.0456 · Cited by 914
Estrogen, cytokines, and pathogenesis of postmenopausal osteoporosis
Pacifici, R. (1996) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.5650110802 · Cited by 741
MicroRNAs: key regulators of stem cells
Gangaraju, V. K., & Lin, H. (2009) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2621 · Cited by 734
Estrogen deficiency induces bone loss by enhancing T-cell production of TNF-α
Cenci, S., Weitzmann, M. N., Roggia, C., Namba, N., Novack, D., Woodring, J., & Pacifici, R. (2000) · Journal of Clinical Investigation · doi:10.1172/jci11066 · Cited by 705
MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis
Kurowska-Stolarska, M., Alivernini, S., Ballantine, L. E., Asquith, D. L., Millar, N. L., Gilchrist, D. S., Reilly, J., Ierna, M., Fraser, A. R., Stolarski, B., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1019536108 · Cited by 641
Cited by
Five Freely Circulating miRNAs and Bone Tissue miRNAs Are Associated With Osteoporotic Fractures
Seeliger, C., Karpinski, K., Haug, A. T., Vester, H., Schmitt, A., Bauer, J. S., & van Griensven, M. (2014) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.2175 · Cited by 329
miR-21 deficiency inhibits osteoclast function and prevents bone loss in mice
Hu, C.-H., Sui, B.-D., Du, F.-Y., Shuai, Y., Zheng, C.-X., Zhao, P., Yu, X.-R., & Jin, Y. (2017) · Scientific Reports · doi:10.1038/srep43191 · Cited by 127
Self-citationGuo, J., Wang, F., Hu, Y., Luo, Y., Wei, Y., Xu, K., Zhang, H., Liu, H., Bo, L., Lv, S., et al. (2023) · Cell Reports Medicine · doi:10.1016/j.xcrm.2022.100881 · Cited by 126
High-Dose TGF-β1 Impairs Mesenchymal Stem Cell–Mediated Bone Regeneration via Bmp2 Inhibition
Xu, J., Liu, J., Gan, Y., Dai, K., Zhao, J., Huang, M., Huang, Y., Zhuang, Y., & Zhang, X. (2020) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.3871 · Cited by 68
Chen, Y.-C., Hsu, P.-Y., Su, M.-C., Chin, C.-H., Liou, C.-W., Wang, T.-Y., Lin, Y.-Y., Lee, C. P., Lin, M.-C., & Hsiao, C.-C. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21030999 · Cited by 32
Metadata
- Authors
- Yang, N., Wang, G., Hu, C., Shi, Y., Liao, L., Shi, S., Cai, Y., Cheng, S., Wang, X., Liu, Y., Tang, L., Ding, Y., & Jin, Y.
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-10-16
- Volume
- 28
- Issue
- 3
- Pages
- 559-573
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- OpenAlex
- W2080109550
- Cited by
- 255
- References
- 70
- FWCI
- 4.65
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Yang, N., Wang, G., Hu, C., Shi, Y., Liao, L., Shi, S., Cai, Y., Cheng, S., Wang, X., Liu, Y., Tang, L., Ding, Y., & Jin, Y. (2013). Tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter miR-21 in estrogen deficiency–induced osteoporosis. Journal of Bone and Mineral Research. https://doi.org/10.1002/jbmr.1798
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