CUX1 attenuates the apoptosis of renal tubular epithelial cells induced by contrast media through activating the PI3K/AKT signaling pathway.


Journal

BMC nephrology
ISSN: 1471-2369
Titre abrégé: BMC Nephrol
Pays: England
ID NLM: 100967793

Informations de publication

Date de publication:
07 Jun 2024
Historique:
received: 29 06 2023
accepted: 28 05 2024
medline: 8 6 2024
pubmed: 8 6 2024
entrez: 7 6 2024
Statut: epublish

Résumé

Contrast media (CM) is a commonly applied drug in medical examination and surgery. However, contrast-induced acute kidney injury (CIAKI) poses a severe threat to human life and health. Notably, the CUT-like homeobox 1 (CUX1) gene shows protective effects in a variety of cells. Therefore, the objective of this study was to provide a new target for the treatment of CIAKI through exploring the role and possible molecular mechanism of CUX1 in CIAKI. Blood samples were collected from 20 patients with CIAKI and healthy volunteers. Human kidney 2 (HK-2) cells were incubated with 200 mg/mL iohexol for 6 h to establish a contrast-induced injury model of HK-2 cells. Subsequently, qRT-PCR was used to detect the relative mRNA expression of CUX1; CCK-8 and flow cytometry to assess the proliferation and apoptosis of HK-2 cells; the levels of IL(interleukin)-1β, tumor necrosis factor alpha (TNF-α) and malondialdehyde (MDA) in cells and lactate dehydrogenase (LDH) activity in cell culture supernatant were detect; and western blot to observe the expression levels of CUX1 and the PI3K/AKT signaling pathway related proteins [phosphorylated phosphoinositide 3-kinase (p-PI3K), PI3K, phosphorylated Akt (p-AKT), AKT]. CUX1 expression was significantly downregulated in blood samples of patients with CIAKI and contrast-induced HK-2 cells. Contrast media (CM; iohexol) treatment significantly reduced the proliferation of HK-2 cells, promoted apoptosis, stimulated inflammation and oxidative stress that caused cell damage. CUX1 overexpression alleviated cell damage by significantly improving the proliferation level of HK-2 cells induced by CM, inhibiting cell apoptosis, and reducing the level of LDH in culture supernatant and the expression of IL-1β, TNF-α and MDA in cells. CM treatment significantly inhibited the activity of PI3K/AKT signaling pathway activity. Nevertheless, up-regulating CUX1 could activate the PI3K/AKT signaling pathway activity in HK-2 cells induced by CM. CUX1 promotes cell proliferation, inhibits apoptosis, and reduces inflammation and oxidative stress in CM-induced HK-2 cells to alleviate CM-induced damage. The mechanism of CUX1 may be correlated with activation of the PI3K/AKT signaling pathway.

Identifiants

pubmed: 38849771
doi: 10.1186/s12882-024-03625-8
pii: 10.1186/s12882-024-03625-8
doi:

Substances chimiques

Contrast Media 0
Proto-Oncogene Proteins c-akt EC 2.7.11.1
Phosphatidylinositol 3-Kinases EC 2.7.1.-
Homeodomain Proteins 0
CUX1 protein, human 0
Transcription Factors 0
Iohexol 4419T9MX03
Repressor Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

192

Informations de copyright

© 2024. The Author(s).

Références

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Auteurs

Rong-Zheng Yue (RZ)

Department of Nephrology, Kindey Research Institute, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.

Jing Wang (J)

Department of Nephrology, Kindey Research Institute, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.

Feng Lin (F)

Department of Nephrology, Kindey Research Institute, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.

Cong-Jun Li (CJ)

Department of Nephrology, Kindey Research Institute, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.

Bai-Hai Su (BH)

Department of Nephrology, Kindey Research Institute, West China Hospital of Sichuan University, Chengdu, Sichuan, 610041, China.

Rui Zeng (R)

Department of Cardiovascular diseases, West China Hospital, School of Clinic Medicine, Sichuan University, Chengdu, Sichuan, 610041, China. 13518160346@163.com.

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