Open Access

Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4

  • Authors:
    • Jing-Meng Hu
    • Li-Jie He
    • Peng-Bo Wang
    • Yan Yu
    • Ya-Ping Ye
    • Li Liang
  • View Affiliations

  • Published online on: July 9, 2021     https://doi.org/10.3892/ijmm.2021.5002
  • Article Number: 169
  • Copyright: © Hu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute renal injury (ARI) is a life‑threatening condition and a main contributor to end‑stage renal disease, which is mainly caused by ischemia‑reperfusion (I/R). miR‑106b‑5p is a kidney function‑related miRNA; however, whether miR‑106b‑5p regulates the progression of ARI remains unclear. The present study thus aimed to examine the effects of miR‑106b‑5p antagonist on the regulation of ARI progression. It was found that miR‑106b‑5p expression was upregulated in the renal tissue of rats with I/R‑induced ARI and in NRK‑52E rat renal proximal tubular epithelial cells subjected to hypoxia‑reoxygenation (H/R). In vitro, H/R induction suppressed the proliferation, and promoted the apoptosis and autophagy of NRK‑52E cells, whereas miR‑106b‑5p antagonist (inhibition of miR‑106b‑5p) promoted the proliferation, and attenuated the apoptosis and autophagy of NRK‑52E cells under the H/R condition. Dual luciferase reporter gene assay validated that transcription factor 4 (TCF4) was a target of miR‑106b‑5p. It was further found that TCF4 overexpression promoted the proliferation, and inhibited the apoptosis and autophagy of NRK‑52E cells subjected to H/R. Moreover, the effects of miR‑106b‑5p antagonist on NRK‑52E cell proliferation, apoptosis and autophagy were mediated through the regulation of TCF4. In vivo, miR‑106b‑5p antagonist reduced the severity of renal injury, decreased cell proliferation in renal tissues and lowered the serum creatinine (Scr) and blood urea nitrogen (BUN) levels in the blood samples from rats with I/R‑induced ARI. On the whole, the findings presented herein demonstrate that miR‑106b‑5p antagonist attenuates ARI by promoting the proliferation, and suppressing the apoptosis and autophagy of renal cells via upregulating TCF4.
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September-2021
Volume 48 Issue 3

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Hu J, He L, Wang P, Yu Y, Ye Y and Liang L: Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4. Int J Mol Med 48: 169, 2021
APA
Hu, J., He, L., Wang, P., Yu, Y., Ye, Y., & Liang, L. (2021). Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4. International Journal of Molecular Medicine, 48, 169. https://doi.org/10.3892/ijmm.2021.5002
MLA
Hu, J., He, L., Wang, P., Yu, Y., Ye, Y., Liang, L."Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4". International Journal of Molecular Medicine 48.3 (2021): 169.
Chicago
Hu, J., He, L., Wang, P., Yu, Y., Ye, Y., Liang, L."Antagonist targeting miR‑106b‑5p attenuates acute renal injury by regulating renal function, apoptosis and autophagy via the upregulation of TCF4". International Journal of Molecular Medicine 48, no. 3 (2021): 169. https://doi.org/10.3892/ijmm.2021.5002