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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. [ABSTRACT FROM AUTHOR]

Background In previous studies we found that miR-125b was down-regulated in denatured dermis of deep partial thickness burn patients. Moreover, miR-125b inhibited tumor-angiogenesis associated with the decrease of ERBB2 and VEGF expression in ovarian cancer cells and breast cancer cells, etc. In this study, we investigated the expression patterns and roles of miR-125b during the recovery of denatured dermis and heat-denatured human umbilical vein endothelial cells (HUVECs). Methods Deep partial thickness burns in Sprague–Dawley rats and the heat-denatured cells (52 °C, 35 s) were used for analysis. Western blot analysis and real-time PCR were applied to evaluate the expression of miR-125b and ERBB2 and VEGF. The ability of angiogenesis in heat-denatured HUVECs was analyzed by scratch wound healing and tube formation assay after pri-miR-125b or anti-miR-125b transfection. Results miR-125b expression was time-dependent during the recovery of heat-denatured dermis and HUVECs. Moreover, miR-125b regulated ERBB2 mRNA and Protein Expression and regulated angiogenesis association with regulating the expression of VEGF in heat-denatured HUVECs. Conclusions Taken together our results show that the expression of miR-125b is time-dependent and miR-125b plays a regulatory role of angiogenesis during wound healing after burns. [ABSTRACT FROM AUTHOR]