The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
miR-100-5p-abundant exosomes derived from infrapatellar fat pad MSCs protect articular cartilage and ameliorate gait abnormalities via inhibition of mTOR in osteoarthritis
Abstract
Osteoarthritis (OA) is the most common disabling joint disease throughout the world and its therapeutic effect is still not satisfactory in clinic nowadays. Recent studies showed that the exosomes derived from several types of mesenchymal stem cells (MSCs) could maintain chondrocyte homeostasis and ameliorate the pathological severity of OA in animal models, indicating that MSCs-derived exosomes could be a novel promising strategy for treating OA. In this study, we investigated the role and underlying mechanisms of infrapatellar fat pad (IPFP) MSCs-derived exosomes (MSCIPFP-Exos) on OA in vitro and in vivo. Our data revealed that MSCIPFP could produce amounts of MSCIPFP-Exos, which exhibited the typical morphological features of exosomes. The MSCIPFP-Exos ameliorated the OA severity in vivo and inhibited cell apoptosis, enhanced matrix synthesis and reduced the expression of catabolic factor in vitro. Moreover, MSCIPFP-Exos could significantly enhance autophagy level in chondrocytes partially via mTOR inhibition. Exosomal RNA-seq showed that the level of miR-100-5p that could bind to the 3'-untranslated region (3'UTR) of mTOR was the highest among microRNAs. MSCIPFP-Exos decreased the luciferase activity of mTOR 3'UTR, while inhibition of miR-100-5p could reverse the MSCIPFP-Exos-decreased mTOR signaling pathway. Intra-articular injection of antagomir-miR-100-5p dramatically attenuated MSCIPFP-Exos-mediated protective effect on articular cartilage in vivo. In brief, MSCIPFP-derived exosomes protect articular cartilage from damage and ameliorate gait abnormality in OA mice by maintaining cartilage homeostasis, the mechanism of which may be related to miR100-5p-regulated inhibition of mTOR-autophagy pathway. As it is relatively feasible to obtain human IPFP from OA patients by arthroscopic operation in clinic, MSCIPFP-derived exosomes may be a potential therapy for OA in the future.
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Cites
MTOR: a pharmacologic target for autophagy regulation
Kim, Y. C., & Guan, K.-L. (2015) · Journal of Clinical Investigation · doi:10.1172/jci73939 · Cited by 2,126
Inflammation in osteoarthritis
Goldring, M. B., & Otero, M. (2011) · Current Opinion in Rheumatology · doi:10.1097/bor.0b013e328349c2b1 · Cited by 1,462
Exosomes: Vehicles of Intercellular Signaling, Biomarkers, and Vectors of Cell Therapy
Kourembanas, S. (2015) · Annual Review of Physiology · doi:10.1146/annurev-physiol-021014-071641 · Cited by 761
Caramés, B., Taniguchi, N., Otsuki, S., Blanco, F. J., & Lotz, M. (2010) · Arthritis & Rheumatism · doi:10.1002/art.27305 · Cited by 632
Subchondral bone osteoclasts induce sensory innervation and osteoarthritis pain
Zhu, S., Zhu, J., Zhen, G., Hu, Y., An, S., Li, Y., Zheng, Q., Chen, Z., Yang, Y., Wan, M., et al. (2019) · Journal of Clinical Investigation · doi:10.1172/jci121561 · Cited by 456
Autophagy and cartilage homeostasis mechanisms in joint health, aging and OA
Lotz, M. K., & Caramés, B. (2011) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2011.109 · Cited by 314
Autophagy modulates osteoarthritis‐related gene expression in human chondrocytes
Sasaki, H., Takayama, K., Matsushita, T., Ishida, K., Kubo, S., Matsumoto, T., Fujita, N., Oka, S., Kurosaka, M., & Kuroda, R. (2012) · Arthritis & Rheumatism · doi:10.1002/art.34323 · Cited by 266
Genetic epidemiology of hip and knee osteoarthritis
Valdes, A. M., & Spector, T. D. (2011) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2010.191 · Cited by 256
The Influence of Aging on the Regenerative Potential of Human Adipose Derived Mesenchymal Stem Cells
Marędziak, M., Marycz, K., Tomaszewski, K. A., Kornicka, K., & Henry, B. M. (2016) · Stem Cells International · doi:10.1155/2016/2152435 · Cited by 225
Vasheghani, F., Zhang, Y., Li, Y.-H., Blati, M., Fahmi, H., Lussier, B., Roughley, P., Lagares, D., Endisha, H., Saffar, B., et al. (2015) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2014-205743 · Cited by 221
Cited by
Osteoarthritis: pathogenic signaling pathways and therapeutic targets
Yao, Q., Wu, X., Tao, C., Gong, W., Chen, M., Qu, M., Zhong, Y., He, T., Chen, S., & Xiao, G. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01330-w · Cited by 1,194
Clinical applications of stem cell-derived exosomes
Tan, F., Li, X., Wang, Z., Li, J., Shahzad, K., & Zheng, J. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01704-0 · Cited by 708
Self-citationKou, M., Huang, L., Yang, J., Chiang, Z., Chen, S., Liu, J., Guo, L., Zhang, X., Zhou, X., Xu, X., et al. (2022) · Cell Death & Disease · doi:10.1038/s41419-022-05034-x · Cited by 640
Self-citationZhang, F.-X., Liu, P., Ding, W., Meng, Q.-B., Su, D.-H., Zhang, Q.-C., Lian, R.-X., Yu, B.-Q., Zhao, M.-D., Dong, J., et al. (2021) · Biomaterials · doi:10.1016/j.biomaterials.2021.121169 · Cited by 328
Hu, H., Dong, L., Bu, Z., Shen, Y., Luo, J., Zhang, H., Zhao, S., Lv, F., & Liu, Z. (2020) · Journal of Extracellular Vesicles · doi:10.1080/20013078.2020.1778883 · Cited by 310
Metadata
- Authors
- Wu, J., Kuang, L., Chen, C., Yang, J., Zeng, W.-N., Li, T., Chen, H., Huang, S., Fu, Z., Li, J., Liu, R., Ni, Z., Chen, L., & Yang, L.
- Venue
- Biomaterials
- Publisher
- Elsevier BV
- Published
- 2019-06
- Volume
- 206
- Pages
- 87-100
- ISSN
- 0142-9612 (ISSN-L)
- OpenAlex
- W2923441281
- Cited by
- 570
- References
- 11
- FWCI
- 41.11
- Type
- journal article
- Language
- en
- Open access
- closed
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- Wu, J., Kuang, L., Chen, C., Yang, J., Zeng, W.-N., Li, T., Chen, H., Huang, S., Fu, Z., Li, J., Liu, R., Ni, Z., Chen, L., & Yang, L. (2019). miR-100-5p-abundant exosomes derived from infrapatellar fat pad MSCs protect articular cartilage and ameliorate gait abnormalities via inhibition of mTOR in osteoarthritis. Biomaterials. https://doi.org/10.1016/j.biomaterials.2019.03.022
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