Our previous study confirmed the critical role of miR‐125b and vascular endothelial growth factor (VEGF) in burn wound repair., The present study was aimed to identify the role of long noncoding RNAs (lncRNAs) related to the function of miR‐125b and VEGF in burn wound repair and the underlying mechanism. First, we found that lncRNA PDK1‐AS and VEGFA expression was significantly increased in heat‐denatured dermal tissue samples and in human dermal microvascular endothelial cells (HDMECs) and human umbilical vein endothelial cells (HUVECs) after thermal injury. PDK1‐AS knockdown significantly inhibited cell viability, cumulative tube length, cell migratory ability, and cell invasion of thermally injured HDMECs and HUVECs. PDK1‐AS knockdown decreased VEGFA protein levels in HDMECs and HUVECs. While overexpression of PDK1‐AS showed the opposite effects. Online tools prediction and luciferase assay confirmed that miR‐125b‐5p targeted PDK1‐AS and VEGFA 3′‐untranslated region. miR‐125b‐5p inhibition significantly increased VEGFA protein levels and enhanced viability, cumulative tube length, migratory ability, and invasion of HUVECs and HDMECs. Furthermore, the effects of PDK1‐AS knockdown on VEGFA protein levels in the two cell lines were partially reversed by miR‐125b‐5p inhibition. Finally, in the tissue samples, PDK1‐AS and VEGFA expression was increased, while miR‐125b‐5p expression was decreased in heat‐denatured dermal tissues; the expression of miR‐125b‐5p had a negative correlation with PDK1‐AS and VEGFA, respectively, and PDK1‐AS and VEGFA were positively correlated with each other in tissue samples. In conclusion, PDK1‐AS relieves miR‐125b‐5p‐induced inhibition on VEGFA by acting as a endogenous RNA, therefore modulating HDMEC and HUVEC angiogenesis after thermal injury.

中文翻译：

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长链非编码 RNA PDK1-AS/miR-125b-5p/VEGFA 轴调节热损伤后人真皮微血管内皮细胞和人脐静脉内皮细胞血管生成

我们之前的研究证实了 miR-125b 和血管内皮生长因子 (VEGF) 在烧伤修复中的关键作用。本研究旨在确定与 miR-125b 和VEGF 在烧伤创面修复中的作用及其潜在机制。首先，我们发现lncRNA PDK1-AS和VEGFA在热变性真皮组织样本、人真皮微血管内皮细胞（HDMECs）和人脐静脉内皮细胞（HUVECs）中的表达在热损伤后显着增加。PDK1-AS 敲低显着抑制热损伤 HDMEC 和 HUVEC 的细胞活力、累积管长度、细胞迁移能力和细胞侵袭。PDK1-AS 敲低降低了 HDMEC 和 HUVEC 中的 VEGFA 蛋白水平。而过表达 PDK1-AS 显示出相反的效果。在线工具预测和荧光素酶测定证实 miR-125b-5p 靶向 PDK1-AS 和 VEGFA 3'-非翻译区。miR-125b-5p 抑制显着增加了 VEGFA 蛋白水平，并增强了 HUVEC 和 HDMEC 的生存力、累积管长度、迁移能力和侵袭。此外，抑制 PDK1-AS 对两种细胞系中 VEGFA 蛋白水平的影响被 miR-125b-5p 抑制部分逆转。最后，在组织样本中，热变性真皮组织中PDK1-AS和VEGFA表达增加，而miR-125b-5p表达降低；miR-125b-5p的表达分别与PDK1-AS和VEGFA呈负相关，组织样本中PDK1-AS和VEGFA呈正相关。综上所述，