Exosomal‑miR‑1184 derived from mesenchymal stem cells alleviates cisplatin‑associated acute kidney injury Corrigendum in /10.3892/mmr.2022.12757

Zhang,Jinshi; He,Wenfang; Zheng,Danna; He,Qiang; Tan,Mingming; Jin,Juan

doi:10.3892/mmr.2021.12435

Exosomal‑miR‑1184 derived from mesenchymal stem cells alleviates cisplatin‑associated acute kidney injury

Corrigendum in: /10.3892/mmr.2022.12757

Authors:
- Jinshi Zhang
- Wenfang He
- Danna Zheng
- Qiang He
- Mingming Tan
- Juan Jin
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Affiliations: Department of Nephrology, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China, Department of Quality Management, Zhejiang Provincial People's Hospital, Hangzhou, Zhejiang 310014, P.R. China
Published online on: September 13, 2021 https://doi.org/10.3892/mmr.2021.12435
Article Number: 795
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute kidney injury (AKI) poses a severe threat to human health. MicroRNAs (miRNAs/miRs) are known to be involved in the progression of AKI; however, the function of miR‑1184 in AKI remains unclear. Thus, the aim of the present study was to examine the role of this miRNA in kidney injury. In order to mimic AKI in vitro, HK‑2 cells were treated with cisplatin. Bioinformatics analysis was performed to explore the differentially expressed miRNAs in AKI. A Cell Counting Kit‑8 assay and flow cytometry were performed to examine cell viability and apoptosis, respectively. mRNA expression levels were detected via reverse transcription‑quantitative PCR, and protein levels were investigated by western blot analysis. ELISA was performed to examine the levels of IL‑1β and TNF‑α in the cell supernatants. The results revealed that miR‑1184 expression was downregulated in AKI. Exosomes derived from miR‑1184 agomir‑treated mesenchymal stem cells (MSCs) significantly reversed cisplatin‑induced cell growth inhibition by inhibiting apoptosis. Moreover, forkhead box O4 (FOXO4) was found to be the direct target of miR‑1184, and exosomes expressing miR‑1184 notably inhibited cisplatin‑induced inflammatory responses in HK‑2 cells via the mediation of IL‑1β and TNF‑α. Furthermore, exosomes derived from miR‑1184 agomir‑treated MSCs significantly induced G1 phase arrest in HK‑2 cells via the regulation of FOXO4, p27 Kip1 and CDK2. In conclusion, the present study demonstrated that exosomal‑miR‑1184 derived from MSCs alleviates cisplatin‑associated AKI. Thus, the findings presented herein may shed new light onto the exploration of novel strategies for the treatment of AKI.

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