生物
上皮
病理
干细胞
转录组
免疫染色
肠粘膜
离体
类有机物
溃疡性结肠炎
炎症性肠病
潘尼斯电池
肠上皮
免疫学
基因表达
免疫组织化学
医学
疾病
内科学
体内
基因
细胞生物学
小肠
生物化学
生物技术
作者
Isabella Dotti,Rut Mora-Buch,Elena Ferrer-Picón,Núria Planell,Peter Jung,Maria Carme Masamunt,Raquel Franco Leal,Javier Martín de Carpi,Josep Llach,Íngrid Ordás,Eduard Batlle,Julián Panés,Antonio Salas
出处
期刊:Gut
[BMJ]
日期:2016-11-01
卷期号:66 (12): 2069-2079
被引量:146
标识
DOI:10.1136/gutjnl-2016-312609
摘要
UC is a chronic inflammatory disease of the colonic mucosa. Growing evidence supports a role for epithelial cell defects in driving pathology. Moreover, long-lasting changes in the epithelial barrier have been reported in quiescent UC. Our aim was to investigate whether epithelial cell defects could originate from changes in the epithelial compartment imprinted by the disease.Epithelial organoid cultures (EpOCs) were expanded ex vivo from the intestinal crypts of non-IBD controls and patients with UC. EpOCs were induced to differentiate (d-EpOCs), and the total RNA was extracted for microarray and quantitative real-time PCR (qPCR) analyses. Whole intestinal samples were used to determine mRNA expression by qPCR, or protein localisation by immunostaining.EpOCs from patients with UC maintained self-renewal potential and the capability to give rise to differentiated epithelial cell lineages comparable with control EpOCs. Nonetheless, a group of genes was differentially regulated in the EpOCs and d-EpOCs of patients with UC, including genes associated with antimicrobial defence (ie, LYZ, PLA2G2A), with secretory (ie, ZG16, CLCA1) and absorptive (ie, AQP8, MUC12) functions, and with a gastric phenotype (ie, ANXA10, CLDN18 and LYZ). A high rate of concordance was found in the expression profiles of the organoid cultures and whole colonic tissues from patients with UC.Permanent changes in the colonic epithelium of patients with UC could be promoted by alterations imprinted in the stem cell compartment. These changes may contribute to perpetuation of the disease.
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