High glucose promotes hepatic fibrosis via miR-32/MTA3-mediated epithelial-to-mesenchymal transition
High glucose promotes hepatic fibrosis via miR-32/MTA3-mediated epithelial-to-mesenchymal transition
复制标题
高糖通过 miR-32/MTA3 介导的上皮间质转化促进肝纤维化
DOI：
10.3892/mmr.2019.9986
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发表时间：
2019-04-01
影响因子：
3.4
通讯作者：
Zhang, Yong
中科院分区：
文献类型：
--
作者：
Li, Qiang;Li, Zhange;Zhang, Yong
肝纤维化的特征是细胞外基质（ECM）蛋白的异常产生和沉积。越来越多的证据表明，上皮-间质转化在肝纤维化的进展中起着至关重要的作用。虽然最近已经确定了一个小分子RNA（miRNAs或miRs）的子集作为EMT基因表达的重要调节因子，但对EMT在高血糖诱导的肝纤维化中的研究有限。本研究观察到高糖处理的AML 12细胞发生EMT过程，miR-32在链脲佐菌素诱导的糖尿病大鼠肝组织和高糖处理的AML 12细胞中表达明显增加。此外，在高血糖条件下，通过靶向转移相关基因3（MTA 3），EMT对肝纤维化的贡献被AMO-32抑制。结果表明，miR-32和MTA 3可能成为防治高血糖状态下肝纤维化的新药物靶点。这些发现提高了对肝纤维化进展的认识。
Hepatic fibrosis is characterized by the aberrant production and deposition of extracellular matrix (ECM) proteins. Growing evidence indicates that the epithelial-mesenchymal transition serves a crucial role in the progression of liver fibrogenesis. Although a subset of microRNAs (miRNAs or miRs) has recently been identified as essential regulators of the EMT gene expression, studies of the EMT in hyperglycemic-induced liver fibrosis are limited. In the current study, it was observed that high glucose-treated AML12 cells occurred EMT process, and miR-32 expression was markedly increased in the liver tissue of streptozotocin-induced diabetic rats and in high glucose-treated AML12 cells. Additionally, the contribution of the EMT to liver fibrosis by targeting metastasis-associated gene 3 (MTA3) under hyperglycemic conditions was suppressed by AMO-32. The results indicated that miR-32 and MTA3 may be considered as novel drug targets in the prevention and treatment of liver fibrosis under hyperglycemic conditions. These finding improves the understanding of the progression of liver fibrogenesis.