Previous studies have identified abnormal expression of lncRNA SNHG12 in ischemic stroke, but the underlying molecular mechanism remains unclear. Through database predictions, m6A methylation sites were found on SNHG12, suggesting post-transcriptional modification. To further elucidate the role of SNHG12 and m6A methyltransferase WTAP in oxygen-glucose deprivation/reperfusion (OGD/R)-induced damage in cerebral microvascular endothelial cells, we conducted investigations. Additionally, we examined the impact of m6A methyltransferase WTAP on SNHG12 expression. Overexpressing SNHG12 in bEnd.3 cells was found to inhibit cell proliferation and promote apoptosis, as well as activate the production of reactive oxygen species and inflammatory cytokines (E-selectin, IL-6 and MCP-1), along with angiogenic proteins (VEGFA and FGFb). Conversely, SNHG12 knockdown alleviated OGD/R-induced damage to BEnd.3 cells, resulting in improved cell proliferation, reduced apoptosis, decreased ROS and LDH production, as well as diminished expression of inflammatory cytokines (E-selectin, IL-6 and MCP-1) and angiogenic proteins (VEGFA and FGFb). Furthermore, WTAP was found to positively regulate SNHG12 expression, and WTAP knockdown in bEnd.3 cells under the OGD/R conditions inhibited cell proliferation, promoted apoptosis, and increased ROS and LDH production. These findings suggest that WTAP may play a crucial role in SNHG12-mediated OGD/R-induced damage in bEnd.3 cells. More molecular experiments are needed to further analyze its mechanism. Overall, our study helps to enrich our understanding of the dysregulation of SNHG12 in ischemic stroke.

中文翻译：

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WTAP调控的LncRNA SNHG12加重bEnd.3细胞氧糖剥夺/再灌注损伤

先前的研究已发现lncRNA SNHG12在缺血性脑卒中中的异常表达，但其潜在的分子机制仍不清楚。通过数据库预测，在SNHG12上发现了m6A甲基化位点，表明存在转录后修饰。为了进一步阐明 SNHG12 和 m6A 甲基转移酶 WTAP 在氧糖剥夺/再灌注 (OGD/R) 诱导的脑微血管内皮细胞损伤中的作用，我们进行了研究。此外，我们还检查了 m6A 甲基转移酶 WTAP 对 SNHG12 表达的影响。研究发现，bEnd.3 细胞中过度表达 SNHG12 可抑制细胞增殖并促进细胞凋亡，并激活活性氧和炎症细胞因子（E-选择素、IL-6 和 MCP-1）以及血管生成蛋白 (VEGFA) 的产生。和 FGFb)。相反，SNHG12 敲低减轻了 OGD/R 诱导的 BEnd.3 细胞损伤，从而改善细胞增殖、减少细胞凋亡、减少 ROS 和 LDH 产生，以及减少炎症细胞因子（E-选择素、IL-6 和 MCP）的表达-1) 和血管生成蛋白（VEGFA 和 FGFb）。此外，发现 WTAP 可以正向调节 SNHG12 的表达，并且 OGD/R 条件下 bEnd.3 细胞中 WTAP 敲低可抑制细胞增殖，促进细胞凋亡，并增加 ROS 和 LDH 的产生。这些发现表明 WTAP 可能在 SNHG12 介导的 OGD/R 诱导的 bEnd.3 细胞损伤中发挥关键作用。需要更多的分子实验来进一步分析其机制。总的来说，我们的研究有助于丰富我们对缺血性中风中 SNHG12 失调的理解。