Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, No. 24, Heping Road, Xiangfang District, Harbin, 150040, Heilongjiang, China.
Department of Nephrology, The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, 150040, Heilongjiang, China.
Biotechnol Lett. 2021 Feb;43(2):393-405. doi: 10.1007/s10529-020-03045-2. Epub 2020 Nov 9.
Myocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI.
CCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression.
miR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.
心肌梗死（MI）是一种常见的心血管难题，也是疾病导致死亡的主要原因。我们进行这项研究是为了检测潜在重要的 miRNA 或基因在 MI 中的作用。
CCL20 可能是一个潜在的治疗靶点，它直接受到 miR-19a 的靶向调控和负调控。CCL20 在 MI 组织样本中的表达显著增加，但 miR-19a 在 MI 中的表达水平较低。与 Sham 组相比，H/R 处理抑制了细胞活力，并诱导了凋亡率的增加。然而，miR-19a 模拟物减轻了 H/R 刺激对心肌细胞的损伤。在心肌细胞中，miR-19a 对 H/R 的保护作用被 CCL20 的增强所逆转，并且在此过程中 MAPK 信号通路被失活。
miR-19a 通过直接靶向 CCL20 并减弱 MAPK 信号通路的活性，消除了心肌细胞中 H/R 诱导的损伤。这些观察结果强调了 miR-19a 和 CCL20 在 MI 治疗中的治疗作用。
