染色质免疫沉淀
生物
促炎细胞因子
转录因子
长非编码RNA
细胞生物学
基因表达
发起人
分子生物学
核糖核酸
基因
遗传学
炎症
免疫学
作者
Felix R. Jimenez,Courtney H. Ruggiero,Robert J. Cousins
出处
期刊:Nutrients
[MDPI AG]
日期:2022-12-01
卷期号:14 (23): 5114-5114
被引量:2
摘要
Integration of non-coding RNAs and miRNAs with physiological processes in animals, including nutrient metabolism, is an important new focus. Twenty-three transporter proteins control cellular zinc homeostasis. The transporter Zip14 (Slc39a14) responds to proinflammatory stimuli. Using enterocyte-specific Zip14 knockout mice and RNA-sequencing and quantitative polymerase chain reaction (qPCR), we conducted transcriptome profiling of proximal small intestine, where Zip14 is highly expressed, using RNA from whole intestine tissue, isolated intestinal epithelial cells (IECs) and intestinal organoids. H19, U90926, Meg3, Bvht, Pvt1, Neat1 and miR-7027 were among the most highly expressed genes. Enterocyte-specific deletion of Zip14 demonstrated tissue specific expression, as such these changes were not observed with skeletal muscle. Chromatin immunoprecipitation (ChIP) assays of chromatin from isolated intestinal epithelial cells showed that enterocyte-specific Zip14 deletion enhanced binding of proinflammatory transcription factors (TFs) signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa beta (NF-ĸβ) to promoters of H19, Meg3 and U90926. We conclude enterocyte-specific ablation of Zip14 restricts changes in those RNAs to the intestine. Binding of proinflammatory TFs, NF-ĸβ and STAT3 to the H19, Meg3 and U90926 promoters is consistent with a model where Zip14 ablation, leads to increased TF occupancy, allowing epigenetic regulation of specific lncRNA genes.
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