Clinical Trial
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Upregulation of microRNA‑24 causes vasospasm following subarachnoid hemorrhage by suppressing the expression of endothelial nitric oxide synthase.

MicroRNA (miR)‑24 has been reported to associate with various diseases by acting on different signaling pathways. The present study aimed to elucidate the association between miR‑24 expression levels and vasospasm following subarachnoid hemorrhage (SAH), and its underlying mechanism. An miR online database was searched, identifying endothelial nitric oxide synthase (NOS3) as a potential target gene of miR‑24. A luciferase reporter assay performed to investigate the regulatory association between miR‑24 and NOS3 revealed that miR‑24 bound to the NOS3 3' untranslated region and inhibited NOS3 expression. Reverse transcription‑quantitative polymerase chain reaction and western blot analysis were performed to investigate the miR‑24 and NOS3 expression levels in samples from patients with SAH, and demonstrated a negative correlation between the two. In addition, miR‑24 expression levels were increased in SAH patients with vasospasm compared with those without, whereas the opposite results were observed for NOS3. Vascular smooth muscle cells (VSMCs) transfected with an miR‑24 inhibitor exhibited increased expression levels of NOS3, whereas those transfected with an miR‑24 mimic or NOS3 small interfering RNA exhibited reduced expression levels of NOS3, compared with the control. These results indicated a negative regulatory association between miR‑24 and NOS3. Downregulation of NOS3 may induce vasospasm following SAH, which may be due to the upregualtion of miR‑24 in VSMCs.

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