Research Paper Volume 14, Issue 6 pp 2678—2694

piRNA-6426 increases DNMT3B-mediated SOAT1 methylation and improves heart failure


Figure 8. Overexpression of piRNA-6426 improves cardiomyocyte function in rats with heart failure. The coronary artery occlusion valve was used to establish a HF rat model. piRNA-6426 gene was cloned into the lentiviral vector. And 8×105 TU lentivirus were injected into the HF mice. The rats in each group were anesthetized after feeding for 4 weeks for the detection of various indicators. (A, B) TTC staining was used to detect the infarcted area of rat heart. (C, D) Western blotting was used to detect the expression levels of SOAT1 and DNMT3B proteins. (E, F) The production of ROS was analyzed with DCFH-DA. (G, H) ELISA kits were used to detect LDH activity in heart tissue homogenate and the secretion of serum IL-1β content. (I–L) The rats were anesthetized by intraperitoneal injection of ketamine (100 mg/kg) and xylazine (10 mg/kg), and then placed on XR900 non-invasive blood pressure monitor (Xinruan, Shanghai, China) to monitor and record the heart rate, diastolic arterial pressure (DAP), mean arterial pressure (MAP) and systolic arterial pressure (SAP). (M) RT-qPCR was used to detect the BNP mRNA level in mouse serum. (N, O) ELISA kits were used to detect the secretion of serum TNF-α and BNP levels. (P) The change of DNMT3B bind to the promoter of SOAT1 by chromatin immuno-precipitation (ChIP) method. Values were expressed as mean ± SEM. $ P>0.05, *P<0.05 compared with the sham operation group; ns P>0.05, #P<0.05 compared with the HF group, n=10.