MicroRNA‑1929‑3p participates in murine cytomegalovirus‑induced hypertensive vascular remodeling through Ednra/NLRP3 inflammasome activation.

MicroRNAs (miRNAs) play an important role in the development of vascular remodeling in essential hypertension (EH) by mediating the effects of human cytomegalovirus (HCMV) on the vascular system. Therefore, the aim of the present study was to investigate the effects of murine cytomegalovirus (MCMV) infection on blood pressure and vascular function in mice, in order to elucidate the role of miR‑1929‑3p in this process. For model development, 7‑month‑old C57BL/6J mice were infected with the Smith strain of MCMV, and MCMV DNA, IgG and IgM were detected. Subsequently, blood pressure was measured via the carotid artery, and the morphological changes of the aorta were evaluated by hematoxylin and eosin and Masson's trichrome staining. miR‑1929‑3p transfection was performed using an adeno‑associated virus packaged vector and the changes in vascular structure were then observed. The levels of nitric oxide (NO) and endothelial NO synthase were also assessed with colorimetry. Vascular remodeling and expression of NLRP3 inflammasome pathway‑related proteins were detected by immunohistochemistry and western blotting. Endothelin‑1 (ET‑1), interleukin (IL)‑1β and IL‑18 were assayed by ELISA. The results revealed that MCMV infection increased the blood pressure, promoted vascular remodeling, caused endothelial cell injury, and downregulated miR‑1929‑3p. However, these effects were alleviated by miR‑1929‑3p overexpression, which downregulated endothelin A receptor (Ednra) and NLRP3 inflammasome, as well as endothelial injury‑ and vascular remodeling‑related genes. Taken together, the findings of the present study indicated that overexpression of miR‑1929‑3p may improve MCMV‑induced vascular remodeling, possibly via the deactivation of the NLRP3 inflammasome by ET‑1/Ednra.