Autophagy is activated to protect renal tubular epithelial cells against iodinated contrast mediainduced cytotoxicity.
Mol Med Rep
; 16(6): 8277-8282, 2017 Dec.
Article
en En
| MEDLINE
| ID: mdl-28944925
ABSTRACT
With the steady increase in the use of various contrastrelated technologies in recent years, contrastinduced nephropathy has received significant attention from clinicians and researchers. The present study aimed to determine the potential role of autophagy in iodinated contrast media (CM)induced cell injury and apoptosis in human proximal renal tubular epithelial HK2 cells. The present study used the iodinated CM iohexol (200 mg iodine/ml) to treat HK2 cells for 6 h, in order to establish a damaged cell model. The autophagy inhibitor 3methyladenine (3MA; 10 mM) was used to inhibit the formation of autophagosomes. Immunofluorescence assay and transmission electron microscopy (TEM) were used to observe the formation of autophagosomes in the cytoplasm. The protein expression levels of microtubuleassociated protein 1A/1Blight chain 3 (LC3)II and autophagyrelated protein 7 (Atg7) were detected by western blotting. The cytotoxicity of CM was evaluated by MTT assay and lactate dehydrogenase release, and cell apoptosis was detected by flow cytometry. Increased formation of autophagosomes and autophagic vesicles was observed under TEM in HK2 cells following iohexol treatment for 6 h. Immunofluorescence assay demonstrated that iohexol increased LC3II expression in HK2 cells. Furthermore, the expression levels of LC3II and Atg7 in HK2 cells were significantly upregulated by iohexol administration; however, LC3II and Atg7 expression was decreased by 3MA treatment. These results provided evidence to suggest that autophagy is activated in response to iohexolinduced cell injury and apoptosis, and may exert a renoprotective role in HK2 cells.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Autofagia
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Compuestos de Yodo
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Medios de Contraste
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Células Epiteliales
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Túbulos Renales
Límite:
Humans
Idioma:
En
Revista:
Mol Med Rep
Año:
2017
Tipo del documento:
Article