Sustained cardiac hypertrophy, as previously clarified, serves as a critical initiator of heart failure and therefore is acknowledged as an important factor for heart failure treatment. The broadly demonstrated function and participation of long non-coding RNAs (lncRNAs) in tumors are well accepted. However, the underlying mechanism implicating lncRNAs in cardiac hypertrophy is mostly unexplored and deserves to be specifically studied. The devised work was aimed to disclose the function of lncRNA DS cell adhesion molecule antisense RNA 1 (DSCAM-AS1) in angiotensin II (AngII)-induced cardiac hypertrophy. In this study, we discovered the upregulation of DSCAM-AS1 in cardiomyocytes treated with AngII by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot and qRT-PCR suggested that DSCAM-AS1 silencing attenuated the highly expressed hypertrophic biomarkers including β-myosin heavy chain (β-MHC), brain natriuretic peptide (BNP), and atrial natriuretic peptide (ANP) at mRNA and protein levels. The expanded cell surface in the presence of AngII treatment area was also shrunk by DSCAM-AS1 silencing. Mechanical analysis manifested that DSCAM-AS1 sponged microRNA-188-5p to boost the pro-hypertrophy gene G protein-coupled receptor kinase 2 (GRK2) expression. Rescue experiments unveiled miR-188-5p and GRK2 managed to reverse the anti-hypertrophy impact of DSCAM-AS1 silencing. In summary, DSCAM-AS1 was identified as a positive modulator in cardiac hypertrophy through miR-188-5p decoying and GRK2 augmentation, giving rise to an enriched theoretical basis for finding a promising target in cardiac hypertrophy regulation.

中文翻译：

---

DSCAM-AS1通过吸收miR-188-5p在心脏肥大加重中介导GRK2的促肥大作用。

如前所述，持续的心脏肥大是引起心力衰竭的关键原因，因此被认为是治疗心力衰竭的重要因素。广泛证实的长非编码RNA（lncRNA）在肿瘤中的功能和参与是公认的。然而，牵涉到心肌肥大中的lncRNA的潜在机制大多尚未探索，值得进行专门研究。设计的工作旨在揭示lncRNA DS细胞粘附分子反义RNA 1（DSCAM-AS1）在血管紧张素II（AngII）诱导的心肌肥大中的功能。在这项研究中，我们通过定量实时聚合酶链反应（qRT-PCR）发现了用AngII处理的心肌细胞中DSCAM-AS1的上调。Western印迹和qRT-PCR表明，DSCAM-AS1沉默可在mRNA和蛋白质水平上减弱高表达的肥大生物标志物，包括β-肌球蛋白重链（β-MHC），脑利钠肽（BNP）和心钠素（ANP）。DSCAM-AS1沉默也缩小了存在AngII处理区域的细胞表面。力学分析表明，DSCAM-AS1使microRNA-188-5p海绵化，以增强肥大基因G蛋白偶联受体激酶2（GRK2）的表达。救援实验表明，miR-188-5p和GRK2设法逆转了DSCAM-AS1沉默对肥大的影响。总之，通过miR-188-5p诱变和GRK2增强，DSCAM-AS1被确定为心肌肥大的正调节剂，