MicroRNA-451 increases vascular permeability and suppresses angiogenesis in pulmonary burn injury in a rat model.

BACKGROUND

Burns are common traumas that cause systemic symptoms by increasing vascular permeability.

OBJECTIVES

To investigate the role of miRNA-451 and to clarify the underlying mechanism of the burn process.

MATERIAL AND

METHODS

We established a heat-induced third-degree burn with acute lung injury (ALI) model in rats. Hematoxylin and eosin (H&E) staining and in situ hybridization were performed. Overexpressed miRNA-451 in human umbilical vascular endothelial cells (HUVEC) were carried out. The migration and proliferation of HUVEC cells were examined.

RESULTS

The H&E staining showed that the burn injury caused by heat went through the dermis and damaged deep tissues. Meanwhile, the heat also induced acute lung injury, characterized by inflammatory exudation in the alveoli and significant enlargement of the alveolar septum. In situ hybridization showed that the expression of miRNA-451 increased in the lung endothelial cells. We overexpressed miRNA-451 in human umbilical vascular endothelial cells (HUVEC) and the results showed that miRNA-451 inhibited the migration and proliferation of HUVEC cells, increased HUVEC cell permeability, inhibited cell adhesion, and induced cell apoptosis. Furthermore, the expression of occludin and ZO-1, 2 key protein molecules in forming tight junction between cells, decreased, and the proteins dispersed in the cytoplasm of HUVEC cells.

CONCLUSIONS

MiRNA-451 was upregulated in the lung endothelial cells of the rat model, and contributed to increase lung endothelial cell permeability. It suppresses angiogenesis of lung endothelial cells, indicating their potential as a target in the treatment of burn injuries.