1. Academic Validation
  2. MiR-429 prohibited NF-κB signalling to alleviate contrast-induced acute kidney injury via targeting PDCD4

MiR-429 prohibited NF-κB signalling to alleviate contrast-induced acute kidney injury via targeting PDCD4

  • Autoimmunity. 2021 Aug;54(5):243-253. doi: 10.1080/08916934.2021.1919878.
Hui-Min Niu 1 Li-Qin Guo 1 Yan-Hong Qiao 1 Hai-Yan Jiao 1
Affiliations

Affiliation

  • 1 Department of Nephrology, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, P.R. China.
Abstract

MiR-429 was reported to be downregulated in contrast-induced acute kidney injury (CI-AKI). However, whether miR-429 is functionally relevant with CI-AKI needs further investigation. Human renal tubular epithelial cell (HK-2) cells were stimulated with contrast media iodixanol to establish in vitro CI-AKI model. Cell Counting Kit-8 (CCK-8) was applied to access cell viability. Flow cytometry was performed to determine Apoptosis. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to evaluate level of programmed cell death 4 (PDCD4) mRNA and miR-429 while western blot was applied to evaluate level of proteins including PDCD4, B-cell leukaemia/lymphoma 2 (Bcl-2), BCL2-associated X protein (Bax), cleaved Caspase 3, cleaved Caspase 9, p65, phosphorylated p65. Dual luciferase assay was used to validate miR-429 targeting PDCD4. MiR-429 was downregulated whereas PDCD4 was upregulated in contrast media iodixanol-stimulated HK-2 cells. MiR-429 overexpression elevated cell viability and attenuated cell Apoptosis. Moreover, the activation of nuclear factor kappa-B (NF-κB) signalling was suppressed after miR-429 overexpression, while PDCD4 overexpression reversed these effects. MiR-429 directly targeted PDCD4 and negatively regulated its expression. CI-AKI induced NF-κB signalling activation and PDCD4 overexpression further promoted NF-κB signalling activation. However, the treatment of BAY11-7082 reversed above results. Overexpression of miR-429 attenuated Apoptosis and elevated cell viability in a CI-AKI cell model via targeting PDCD4 and thus restraining NF-κB signalling.

Keywords

NF-κB signalling; PDCD4; acute kidney injury; contrast media; miR-429.

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