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Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells

التفاصيل البيبلوغرافية
العنوان: Apobec-1 Complementation Factor (A1CF) Inhibits Epithelial-Mesenchymal Transition and Migration of Normal Rat Kidney Proximal Tubular Epithelial Cells
المؤلفون: Liyuan Huang, Honglian Wang, Yuru Zhou, Dongsheng Ni, Yanxia Hu, Yaoshui Long, Jianing Liu, Rui Peng, Li Zhou, Zhicheng Liu, Zhongshi Lyu, Zhaomin Mao, Jin Hao, Yiman Li, Qin Zhou
المصدر: International Journal of Molecular Sciences, Vol 17, Iss 2, p 197 (2016)
بيانات النشر: MDPI AG, 2016.
سنة النشر: 2016
المجموعة: LCC:Biology (General)
LCC:Chemistry
مصطلحات موضوعية: A1CF, EMT, kidney tubular epithelial cells, Biology (General), QH301-705.5, Chemistry, QD1-999
الوصف: Apobec-1 complementation factor (A1CF) is a member of the heterogeneous nuclear ribonucleoproteins (hnRNP) family, which participates in site-specific posttranscriptional RNA editing of apolipoprotein B (apoB) transcript. The posttranscriptional editing of apoB mRNA by A1CF in the small intestine is required for lipid absorption. Apart from the intestine, A1CF mRNA is also reported to be highly expressed in the kidneys. However, it is remained unknown about the functions of A1CF in the kidneys. The aim of this paper is to explore the potential functions of A1CF in the kidneys. Our results demonstrated that in C57BL/6 mice A1CF was weakly expressed in embryonic kidneys from E15.5dpc while strongly expressed in mature kidneys after birth, and it mainly existed in the tubules of inner cortex. More importantly, we identified A1CF negatively regulated the process of epithelial-mesenchymal transition (EMT) in kidney tubular epithelial cells. Our results found ectopic expression of A1CF up-regulated the epithelial markers E-cadherin, and down-regulated the mesenchymal markers vimentin and α-smooth muscle actin (α-SMA) in NRK52e cells. In addition, knockdown of A1CF enhanced EMT contrary to the overexpression effect. Notably, the two A1CF variants led to the similar trend in the EMT process. Taken together, these data suggest that A1CF may be an antagonistic factor to the EMT process of kidney tubular epithelial cells.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1422-0067
Relation: http://www.mdpi.com/1422-0067/17/2/197; https://doaj.org/toc/1422-0067
DOI: 10.3390/ijms17020197
URL الوصول: https://doaj.org/article/71f0820c1b7b4ba89f463fea6e4e9386
رقم الأكسشن: edsdoj.71f0820c1b7b4ba89f463fea6e4e9386
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:14220067
DOI:10.3390/ijms17020197