Abstract

Intravenous (IV) infusion of oleic acid (OA) distributes OA microemboli in the pulmonary capillaries, which results in severe vascular congestion, hemorrhage vascular congestion, interstitial edema, intravascular coagulation and bleeding. The immune response to acute lung injury (ALI) is known to be associated with rapid and widespread changes in microRNA (miRNA) expression in the lung. The present study of a model of rat lung injury aimed to investigate how the lung miRNA profile changes to mediate ALI. For the induction of ALI, OA (200µl/kg) suspended in 20% ethyl alcohol was injected through the tail vein for 20min. Lung tissue samples were acquired at 3, 6 and 24h, and miRNA microarray and quantitative polymerase chain reaction were performed using these samples. The activation of phosphatase and tensin homolog (PTEN), protein kinase B (Akt), extracellular signal-regulated kinases (ERK) and c-Jun N-terminal kinases (JNK) were analyzed by western blot analysis. There were 75 miRNAs that demonstrated >1.5‑fold changes in expression levels. miR-101a was highly upregulated at 3h. miR-21 was upregulated in the OA group throughout the 24h following OA challenge. miR-1 was the most downregulated miRNA at 24h. In order to examine the expression levels of PTEN and Akt as targets of miR-21, western blot analysis was performed. At 3h, the levels of PTEN were attenuated in the OA group as compared with those in the control group; however, p-Akt/Akt levels were increased at 3h for the OA group. PTEN and p-Akt/Akt were significantly higher in the OA group at 3h and were rapidly decreased at 6h. The immunohistochemical stain of α-smooth muscle actin in the bronchial and alveolar wall increased 24h after OA‑induced ALI. These results indicated that the profile of miRNAs dynamically changed throughout the OA-induced ALI process, and mitogen-activated protein kinase activation, PTEN/Akt pathway alteration and smooth muscle actin activation were observed in this ALI model.

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