Long non-coding RNA metastasis-related lung adenocarcinoma transcript 1 (MALAT1) forms a negative feedback loop with long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) in sepsis to regulate lung cell apoptosis

长链非编码RNA转移相关肺腺癌转录本1 (MALAT1) 与长链非编码RNA结直肠肿瘤差异表达 (CRNDE) 在脓毒症中形成负反馈环路,从而调节肺细胞凋亡。

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Abstract

It has been reported that long non-coding RNAs (lncRNAs) metastasis-related lung adenocarcinoma transcript 1 (MALAT1) and colorectal neoplasia differentially expressed (CRNDE) play opposite roles in sepsis. Therefore, we explored their potential interaction with sepsis. To this end, we determined MALAT1 and CRNDE levels using RT-qPCR in plasma samples collected from healthy controls (n = 60) and sepsis patients (n = 60) before and after treatment and the effects of MALAT1 and CRNDE overexpression in human bronchial epithelial cells (HBEpCs) on the expression of each other and HBEpC apoptosis. RT-qPCR analyses showed that MALAT1 was upregulated, while CRNDE was downregulated in sepsis and overexpression of MALAT1 and CRNDE downregulated the expression of each other. After proper treatment, MALAT1 was downregulated and CRNDE was upregulated in sepsis. Lipopolysaccharides (LPS) treatment of HBEpCs upregulated MALAT1 and downregulated CRNDE. Cell apoptosis analysis showed that MALAT1 overexpression promoted, while CRNDE overexpression inhibited LPS-induced HBEpC apoptosis. Moreover, CRNDE overexpression attenuated the effects of MALAT1 overexpression. Overall, MALAT1 might form a negative feedback loop with CRNDE in sepsis to regulate lung cell apoptosis.

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