第1章
生物
基因敲除
长非编码RNA
上皮-间质转换
癌症研究
下调和上调
微阵列分析技术
核糖核酸
肾
分子生物学
基因表达
基因
内分泌学
遗传学
作者
Kazuo Imai,Takuji Ishimoto,Tomohito Doke,Takayuki Tsuboi,Yu Watanabe,Keisuke Katsushima,Miho Suzuki,Hideto Oishi,Kazuhiro Furuhashi,Yasuhiko Ito,Yutaka Kondo,Shoichi Maruyama
标识
DOI:10.1016/j.omtn.2022.12.011
摘要
Renal interstitial fibrosis (RIF) is a common pathological manifestation of chronic kidney diseases. Epithelial-mesenchymal transition (EMT) of tubular epithelial cells is considered a major cause of RIF. Although long non-coding RNAs (lncRNAs) are reportedly involved in various pathophysiological processes, the roles and underlying molecular mechanisms of lncRNAs in the progression of RIF are poorly understood. In this study, we investigated the function of lncRNAs in RIF. Microarray assays showed that expression of the lncRNA lnc-CHAF1B-3 (also called claudin 14 antisense RNA 1) was significantly upregulated in human renal proximal tubular cells by both transforming growth factor-β1 (TGF-β1) and hypoxic stimulation, accompanied with increased expression of EMT-related genes. Knockdown of lnc-CHAF1B-3 significantly suppressed TGF-β1-induced upregulated expression of collagen type I alpha 1, cadherin-2, plasminogen activator inhibitor-1, snail family transcriptional repressor I (SNAI1) and SNAI2. Quantitative reverse transcriptase PCR analyses of paraffin-embedded kidney biopsy samples from IgA nephropathy patients revealed lnc-CHAF1B-3 expression was correlated positively with urinary protein levels and correlated negatively with estimated glomerular filtration rate. In situ hybridization demonstrated that lnc-CHAF1B-3 is expressed only in proximal tubules. These findings suggest lnc-CHAF1B-3 affects the progression of RIF by regulating EMT-related signaling. Thus, lnc-CHAF1B-3 is a potential target in the treatment of RIF.
科研通智能强力驱动
Strongly Powered by AbleSci AI