The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Exosome secreted from adipose-derived stem cells attenuates diabetic nephropathy by promoting autophagy flux and inhibiting apoptosis in podocyte
Open accessAbstract
BACKGROUND: It is confirmed that adipose-derived stem cells (ADSCs) transplantation effectively relieves kidney fibrosis and type 2 diabetes disease in mice. Currently, exosome from urine-derived stem cells (USCs) can protect type 1 diabetes-mediated kidney injury and attenuate podocyte damage in diabetic nephropathy (DN). Exosome derived from USCs has evolved into the strategy for DN treatment, but the role of ADSCs-derived exosome (ADSCs-Exo) in DN remains unclear. The present study is aimed to investigate the therapeutic action and molecular mechanism of ADSCs-derived exosome on DN. METHODS: ADSCs and exosome were authenticated by immunofluorescence and flow cytometry. Morphology and the number of exosome were evaluated by electron microscope and Nanosight Tracking Analysis (NTA), respectively. Cell apoptosis was assessed using flow cytometry. Podocyte autophagy and signaling transduction were measured by immunofluorescence and immunoblotting. Dual Luciferase Reporter assay was employed to detect the regulatory relationship between miR-486 and Smad1. RESULTS: ADSCs-Exo attenuated spontaneous diabetes by reducing levels of urine protein, serum creatinine (Scr), blood urea nitrogen (BUN), and podocyte apoptosis in mice. In in vitro experiment, ADSCs-Exo also reversed high glucose-induced decrease of cell viability and the increase of cell apoptosis in MPC5 cells. In terms of mechanism, ADSCs-Exo could enhance autophagy flux and reduce podocyte injury by inhibiting the activation of mTOR signaling in MPC5 and spontaneous diabetic mice. Eventually, we found that miR-486 was the key factors in ADSCs and in the process of ADSCs-Exo-mediated improvement of DN symptom in vivo and in vitro. miR-486 reduced Smad1 expression by target regulating Smad1 whose reduction could inhibit mTOR activation, leading to the increase of autophagy and the reduction of podocyte apoptosis. CONCLUSIONS: In conclusion, we illustrated that ADSCs-Exo vividly ameliorated DN symptom by enhancing the expression of miR-486 which led to the inhibition of Smad1/mTOR signaling pathway in podocyte. Possibly, ADSCs-Exo was used as a main therapeutic strategy for DN in future.
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Kou, 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
Liu, S., Fan, M., Xu, J.-X., Yang, L.-J., Qi, C.-C., Xia, Q.-R., & Ge, J.-F. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02393-2 · Cited by 296
Adipose-derived stem cells secretome and its potential application in “stem cell-free therapy”
Trzyna, A., & Banaś-Ząbczyk, A. (2021) · Biomolecules · doi:10.3390/biom11060878 · Cited by 201
Mesenchymal Stem Cell-Derived Extracellular Vesicles to the Rescue of Renal Injury
Birtwistle, L., Chen, X.-M., & Pollock, C. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126596 · Cited by 113
Diabetes and its complications: molecular mechanisms, prevention and treatment
Zhao, L., Yuan, J., Yang, Q., Ma, J., Yang, F., Zou, Y., Liu, K., & Liu, F. (2026) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02401-w · Cited by 80
Self-citation
Metadata
- Authors
- Jin, J., Shi, Y., Gong, J., Zhao, L., Li, Y., He, Q., & Huang, H.
- Venue
- Stem Cell Research & Therapy
- Published
- 2019-03-15
- Volume
- 10
- Issue
- 1
- Pages
- 95-95
- ISSN
- 1757-6512 (ISSN-L)
- OpenAlex
- W2938394881
- Cited by
- 365
- References
- 42
- FWCI
- 10.60
- Type
- journal article
- Language
- en
- Open access
- gold
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- Jin, J., Shi, Y., Gong, J., Zhao, L., Li, Y., He, Q., & Huang, H. (2019). Exosome secreted from adipose-derived stem cells attenuates diabetic nephropathy by promoting autophagy flux and inhibiting apoptosis in podocyte. Stem Cell Research & Therapy. https://doi.org/10.1186/s13287-019-1177-1
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