Down-regulation of miR-215 attenuates lipopolysaccharide-induced inflammatory injury in CCD-18co cells by targeting GDF11 through the TLR4/NF-κB and JNK/p38 signaling pathways

• Boyang Sun ^[1] ; Kai Xing ^[1] ; Chen Qi ^[1] ; Ke Yan ^[1] ; Yan Xu ^[1]
  1. [1] Nanjing Medical University

     Nanjing Medical University

     China

     
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 35, Nº. 12, 2020, págs. 1473-1481
• Idioma: inglés
• Enlaces
  • Texto completo
• Resumen

  • Ulcerative colitis (UC) is a risk factor for carcinogenesis of colorectal cancer, which is associated with disruption of the epithelial barrier and disorder of the inflammatory response. It has been reported that the expression of microRNA (miR)-215 is upregulated in patients with long-term UC. The present study aimed to investigate the effects of miR-215 on lipopolysaccharide (LPS)-induced inflammatory injury in CCD-18Co cells, as well as to identify the underlying possible molecular mechanisms. CCD-18Co cells were treated with 1 µg/ml LPS to induce inflammatory injury. Reverse transcription-quantitative PCR was performed to determine the expression of miR-215 in LPS-treated CCD-18Co cells. Moreover, a dual luciferase reporter system assay was used to evaluate the interaction of miR-215 and growth differentiation factor 11 (GDF11) in CCD-18Co cells. The expression of miR-215 was significantly upregulated in LPS-treated CCD-18Co cells. Knockdown of miR-215 significantly alleviated the inflammatory response and oxidative stress in LPStreated CCD-18Co cells. In addition, GDF11 was identified as a direct binding target of miR-215 in CCD18Co cells. Knockdown of miR-215 significantly increased the expression of GDF11, but decreased the expression levels of Toll-like receptor (TLR)4, phosphorylated (p)-p65, iNOS, p-p38 and p-JNK in LPS-treated CCD-18Co cells. Collectively, the present findings indicated that knockdown of miR-215 alleviated oxidative stress and inflammatory response in LPStreated CCD-18Co cells by upregulating GDF11 expression and inactivating the TLR4/NF-κB and JNK/p38 signaling pathways