MicroRNA-1297 participates in the repair of intestinal barrier injury in patients with HIV/AIDS via negative regulation of PLCβ1

• Published in: Molecular and cellular biochemistry Vol. 477; no. 8; pp. 2133 - 2147
• Main Authors: Bao, Yuxia, Guo, Huiming, Yang, Bin, Chen, Fengrong, Zhang, Zunyue, Gao, Jianyuan
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.08.2022; Springer Nature B.V
• Subjects: Acquired immune deficiency syndrome; AIDS; Biochemistry; Bioinformatics; Biomedical and Life Sciences; Biosynthesis; Cardiology; Cell viability; Fluorescence; Growth factors; HIV; Human immunodeficiency virus; Immune system; Injuries; Injury analysis; Intestine; Kinases; Life Sciences; Lipopolysaccharides; Localization; Medical Biochemistry; MicroRNAs; miRNA; Oncology; Permeability; Phospholipase C; Proteins; Repair; Signal transduction; Transcriptomes; Transforming growth factor-b; Western blotting; Zonula occludens-1 protein; miRNA; Cell viability; PLCβ1; Intestinal barrier injury
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-022-04426-z

To explore the role of the miRNA-1297/phospholipase Cβ1 (PLCβ1) axis in intestinal barrier injury. Abnormally expressed miR-1297 and its target gene PLCβ1 as well as their transcriptome sequencing were confirmed by bioinformatics analysis. Next, the intestinal barrier injury was induced by lipopolysaccharide (LPS) in the CCCHIE-2 cells. Subsequently, the impacts of miR-1297 and PLCβ1 on the transcriptome were estimated. QRT-PCR and Western blotting were conducted to detect the relative mRNA and protein expressions, respectively. The cell viability and permeability were analyzed by MTT assay and fluorescent yellow detection. miR-1297 was significantly upregulated in patients with human immunodeficiency virus/acquired immunodeficiency syndrome and targeted PLCβ1. Moreover, overexpressed PLCβ1 was mainly enriched in the transforming growth factor-beta signaling pathway, while the knockdown of miR-1297 was focused on the arginine biosynthesis pathway. The overexpression of miR-1297 could reduce the PLCβ1 expression and inhibit the viability of CCCHIE-2 cells injured by LPS, while the effect of the downregulation of miR-1297 was on the opposite. Western blotting and cell fluorescence localization experiments revealed that the inhibition of miR-1297 increased the expressions of PLCβ1 and ZO-1. In addition, the upregulation of miR-1297 strengthened the permeability in cells injured by LPS, as did the knockdown of PLCβ1. miR-1297 could restrain the repair of intestinal barrier injury via negatively regulating PLCβ1 and its tight junction downstream protein ZO-1 in CCC-HIE-2 cells injured by LPS, which indicated that PLCβ1 and miR-1297 might be important targets for the repair of intestinal barrier injury.