Long noncoding ribonucleic acids (lncRNAs) are critical regulators in various biological processes. In the present study, we aimed to explore whether miR140-3p was involved in the underlying molecular mechanisms of small nucleolar RNA host gene 1 (SNHG1) in myocardial ischemia/reperfusion (I/R) injury. A mouse model of I/R injury and hypoxia-reoxygenation (H/R)-stimulated human umbilical vein endothelial cells (HUVECs) was used in this study. Cell proliferation was detected by MTT. The mRNA and protein levels of vascular endothelial growth factor (VEGF), VE-cadherin, and MMP2 were detected by RT-PCR and western blot, respectively. The angiogenesis was assessed by tube formation assay. Cell migration was assessed using wound-healing assay. Results showed that SNHG1 expression was increased in the cardiac microvasculature of a mouse model of I/R injury and in H/R-stimulated HUVECs. H/R stimulation significantly reduced cell proliferation, tube formation, and cell migration, but increased expression of VEGF, VE-cadherin, and MMP2. SNHG1 upregulation under H/R increased HUVECs proliferation, tube formation, and cell migration, and upregulated expression of VEGF, VE-cadherin, and MMP2, compared with the H/R group. SNHG1 knockdown exhibited the opposite effect. SNHG1 functioned as a competing endogenous RNA (ceRNA) of miR-140-3p. HIF-1α was identified as a target of miR-140-3p. SNHG1 upregulation enhanced cell proliferation, tube formation, and expression of VEGF, VE-cadherin, and MMP2 through HIF-1α/VEGF signaling. This process could be offset by miR-140-3p mimic or VEGF inhibitor. Our results reveal a novel protective function of SNHG1 that furthers understanding of cardiac I/R injury and provides experimental evidence for future therapy.

中文翻译：

---

LncRNA SNHG1通过HIF-1α/ VEGF信号通路作为竞争性内源性RNA缓解了缺氧-再氧化引起的血管内皮细胞损伤。

长的非编码核糖核酸（lncRNA）是各种生物过程中的关键调节剂。在本研究中，我们旨在探讨miR140-3p是否参与心肌缺血/再灌注（I / R）损伤的小核仁RNA宿主基因1（SNHG1）的潜在分子机制。在本研究中，使用了I / R损伤和缺氧-复氧（H / R）刺激的人脐静脉内皮细胞（HUVEC）的小鼠模型。通过MTT检测细胞增殖。分别通过RT-PCR和western blot检测血管内皮生长因子（VEGF），VE-钙黏着蛋白和MMP2的mRNA和蛋白水平。通过管形成测定法评估血管生成。使用伤口愈合测定法评估细胞迁移。结果显示，SNHG1表达在I / R损伤小鼠模型和H / R刺激的HUVECs的心脏微血管中增加。H / R刺激显着减少了细胞增殖，管形成和细胞迁移，但增加了VEGF，VE-钙黏着蛋白和MMP2的表达。与H / R组相比，在H / R下SNHG1上调增加了HUVEC的增殖，管形成和细胞迁移，并上调了VEGF，VE-钙黏着蛋白和MMP2的表达。SNHG1组合式显示相反的效果。SNHG1充当miR-140-3p的竞争内源性RNA（ceRNA）。HIF-1α被确定为miR-140-3p的靶标。SNHG1上调通过HIF-1α/ VEGF信号传导增强细胞增殖，管形成以及VEGF，VE-钙黏着蛋白和MMP2的表达。该过程可以被miR-140-3p模拟物或VEGF抑制剂所抵消。