Transcriptomic and Proteomic Profiling Provides Insight into Mesangial Cell Function in IgA Nephropathy

系膜细胞 仿形(计算机编程) 肾病 生物 计算生物学 转录组 细胞生物学 内科学 生物信息学 医学 基因表达 内分泌学 基因 计算机科学 遗传学 糖尿病 操作系统
作者
Peidi Liu,Emelie Lassén,Viji Nair,Céline C. Berthier,Miyuki Suguro,Carina Sihlbom,Matthias Kretzler,Christer Betsholtz,Börje Haraldsson,Wenjun Ju,Kerstin Ebefors,Jenny Nyström
出处
期刊:Journal of The American Society of Nephrology 卷期号:28 (10): 2961-2972 被引量:69
标识
DOI:10.1681/asn.2016101103
摘要

IgA nephropathy (IgAN), the most common GN worldwide, is characterized by circulating galactose-deficient IgA (gd-IgA) that forms immune complexes. The immune complexes are deposited in the glomerular mesangium, leading to inflammation and loss of renal function, but the complete pathophysiology of the disease is not understood. Using an integrated global transcriptomic and proteomic profiling approach, we investigated the role of the mesangium in the onset and progression of IgAN. Global gene expression was investigated by microarray analysis of the glomerular compartment of renal biopsy specimens from patients with IgAN (n=19) and controls (n=22). Using curated glomerular cell type-specific genes from the published literature, we found differential expression of a much higher percentage of mesangial cell-positive standard genes than podocyte-positive standard genes in IgAN. Principal coordinate analysis of expression data revealed clear separation of patient and control samples on the basis of mesangial but not podocyte cell-positive standard genes. Additionally, patient clinical parameters (serum creatinine values and eGFRs) significantly correlated with Z scores derived from the expression profile of mesangial cell-positive standard genes. Among patients grouped according to Oxford MEST score, patients with segmental glomerulosclerosis had a significantly higher mesangial cell-positive standard gene Z score than patients without segmental glomerulosclerosis. By investigating mesangial cell proteomics and glomerular transcriptomics, we identified 22 common pathways induced in mesangial cells by gd-IgA, most of which mediate inflammation. The genes, proteins, and corresponding pathways identified provide novel insights into the pathophysiologic mechanisms leading to IgAN.
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