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. 2021 Oct;44(5):2044-2053.
doi: 10.1007/s10753-021-01480-5. Epub 2021 May 26.

CircANKRD36 Knockdown Suppressed Cell Viability and Migration of LPS-Stimulated RAW264.7 Cells by Sponging MiR-330

Qiqing Lin  1 , Qiong Liang  2 , Chunyan Qin  2 , Yueyong Li  3
Affiliations

CircANKRD36 Knockdown Suppressed Cell Viability and Migration of LPS-Stimulated RAW264.7 Cells by Sponging MiR-330

Qiqing Lin et al. Inflammation. 2021 Oct.

Abstract

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is an independent risk factor for mortality in patients with sepsis. In this study, we attempt to investigate the molecular mechanism of circANKRD36 underlying sepsis-induced ALI/ARDS in vitro. We first detected the altered circRNAs in serums of patients with sepsis-induced ARDS using circRNAs microarray. CircANKRD36 expression in serums and LPS-stimulated RAW264.7 cells was measured using qRT-PCR. CCK-8, cell migration, ELISA, and qRT-PCR were applied to the evaluation of cell biological behavior and inflammation reaction. The results showed that circANKRD36 expression was significantly elevated in serum of patients with sepsis-induced ARDS. Knockdown of circANKRD36 inhibited cell viability and migration and alleviated inflammation of lipopolysaccharide-stimulated (LPS-stimulated) RAW264.7 cells. Bioinformatic analysis demonstrated that circANKRD36 serves as a sponge for miR-330 and ROCK1 was directly targeted by miR-330. Furthermore, knockdown of circANKRD36 repressed ROCK1 expression by targeting miR-330. In short, circANKRD36 knockdown suppressed cell viability and migration of LPS-stimulated RAW264.7 cells in vitro via sponging miR-330, which may provide new ideas for the treatment of sepsis-induced ARDS.

Keywords: ARDS; ROCK1; circANKRD36; miR-330.

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