Heart Center, Aerospace Center Hospital, Beijing, China.
Eur Rev Med Pharmacol Sci. 2019 Oct;23(19):8566-8572. doi: 10.26355/eurrev_201910_19172.
To study the influences of long non-coding ribonucleic acid (lncRNA) X-inactive specific transcript (XIST) on rats with acute myocardial infarction (AMI), and its regulatory mechanism.
A total of 30 Sprague-Dawley rats were randomly assigned into Sham group, Model group, and lncRNA XIST small interfering RNA (XIST siRNA) group. The AMI rat model was prepared through ligating the left anterior descending coronary artery. The left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular systolic diameter (LVDs), and left ventricular diastolic diameter (LVDd) of rats were determined using a color Doppler ultrasound system. Reverse transcription-polymerase chain reaction was performed to measure the expression levels of lncRNA XIST, microRNA (miR)-449, and Notch1 in rat heart tissues in each group. Pathological morphology of rat heart tissues in each group was observed via hematoxylin-eosin (HE) staining. Cell apoptosis in rat heart tissues was evaluated through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.
Compared with those in Sham group, rats in Model group had significantly increased LVEDV, LVESV, LVDs, and LVDd. After transfection with lncRNA XIST siRNA, XIST level in rat heart tissues was remarkably declined in XIST siRNA group compared with that in Model group. According to HE staining results, the pathological injuries in rat heart tissues were greatly improved in XIST siRNA group compared with those in Model group. TUNEL staining results revealed that the apoptosis rate of cells in rat heart tissues in XIST siRNA group was markedly lower than that in Model group. Higher level of miR-449 and lower level of Notch1 were observed in rats of XIST siRNA group than those of Model group.
Knockdown of lncRNA XIST can repress the myocardial cell apoptosis in AMI model rats by downregulating miR-449 level.
研究长非编码 RNA（lncRNA）X 失活特异性转录物（XIST）对急性心肌梗死（AMI）大鼠的影响及其调控机制。
将 30 只 Sprague-Dawley 大鼠随机分为假手术组、模型组和 lncRNA XIST 小干扰 RNA（XIST siRNA）组。结扎大鼠左前降支制备 AMI 大鼠模型。采用彩色多普勒超声系统检测大鼠左心室舒张末期容积（LVEDV）、左心室收缩末期容积（LVESV）、左心室收缩直径（LVDs）和左心室舒张直径（LVDd）。采用逆转录-聚合酶链反应检测各组大鼠心脏组织中 lncRNA XIST、微小 RNA（miR）-449 和 Notch1 的表达水平。苏木精-伊红（HE）染色观察各组大鼠心脏组织的病理形态。末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）法评估大鼠心脏组织细胞凋亡。
与假手术组比较，模型组大鼠的 LVEDV、LVESV、LVDs 和 LVDd 明显增加。转染 lncRNA XIST siRNA 后，XIST siRNA 组大鼠心脏组织中 XIST 水平明显低于模型组。HE 染色结果显示，XIST siRNA 组大鼠心脏组织的病理损伤较模型组明显改善。TUNEL 染色结果显示，XIST siRNA 组大鼠心脏组织细胞凋亡率明显低于模型组。XIST siRNA 组大鼠心脏组织中 miR-449 水平升高，Notch1 水平降低。
下调 lncRNA XIST 可通过下调 miR-449 水平抑制 AMI 模型大鼠心肌细胞凋亡。
