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Article Publish Status: FREE
Abstract Title:

Astragaloside IV Inhibits Galactose-Deficient IgA1 SecretionmiR-98-5p in Pediatric IgA Nephropathy.

Abstract Source:

Front Pharmacol. 2021 ;12:658236. Epub 2021 Apr 16. PMID: 33935780

Abstract Author(s):

Caiqiong Liu, Xiaoyan Li, Lanjun Shuai, Xiqiang Dang, Fangrong Peng, Mingyi Zhao, Shiqiu Xiong, Ying Liu, Qingnan He

Article Affiliation:

Caiqiong Liu

Abstract:

The factor associated with IgA nephropathy (IgAN) is an abnormality of IgA known as galactose-deficient IgA1 (Gd-IgA1). The purpose of this study was to determine the molecular role played by miRNAs in the formation of Gd-IgA1 in IgAN and investigate the regulatory role of Astragaloside IV (AS-IV) in miRNAs.Bioinformatics analysis, along with functional and mechanistic experiments, were used to investigate the relationship and function of miRNA,β-1, 3-galactosyltransferase (C1GALT1), Gd-IgA1, and AS-IV. Analyses involved a series of tools, including quantitative real-time polymerase chain reaction (qRT-qPCR), Western blot, enzyme-linked immunosorbent assay (ELISA), Vicia Villosa lectin-binding assay (VVA), Cell counting kit-8 assay (CCK-8), and the dual-luciferase reporter assay.miRNA screening and validation showed that miR-98-5p was significantly upregulated in the peripheral blood mononuclear cells (PBMCs) of pediatric patients with IgAN compared with patients diagnosed with mesangial proliferative glomerulonephritis (MsPGN) and immunoglobulin A vasculitis nephritis (IgAV-N), and healthy controls (<0.05). Experiments with the dual-luciferase reporter confirmed that miR-98-5p might target C1GALT1. The overexpression of miR-98-5p in DAKIKI cells decreased both the mRNA and protein levels of C1GALT1 and increased the levels of Gd-IgA1 levels; these effects were reversed by co-transfection with the C1GALT1 plasmid, and. In addition, AS-IV downregulated the levels of Gd-IgA1 level in DAKIKI cells by inhibiting miR-98-5p.Our results revealed that AS-IV could inhibit Gd-IgA1 secretionmiR-98-5p. Increased levels of miR-98-5p in pediatric IgAN patients might affect the glycosylation of IgA1 by targeting C1GALT1. In addition, our analyses suggest that the pathogenesis of IgAN may differ from that of IgAV-N. Collectively, these results provide significant insight into the pathogenesis of IgAN and identify a potential therapeutic target.

Study Type : In Vitro Study

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