Exosomal micro ribonucleic acid-154-5p derived from vascular smooth muscle cell mediates intracranial aneurysm phenotype in vitro via myosin light chain kinase targeting.

ObjectiveThe molecular pathogenesis of intracranial aneurysms remains undefined despite its central role in aneurysmal subarachnoid hemorrhage, a major cause of stroke and shock. Although exosomal micro ribonucleic acids have emerged as key regulators in intracranial aneurysm progression, the specific contributions of micro ribonucleic acid-154-5p remain underexplored.MethodsUsing quantitative reverse transcription polymerase chain reaction, we assessed the micro ribonucleic acid-154-5p expression in intracranial aneurysm specimens. Transmission electron microscopy was used to validate the extracted exosome. Exosomal transfer was confirmed using Cy3-labeled micro ribonucleic acid tracing and quantitative reverse transcription polymerase chain reaction. Functional impacts on vascular smooth muscle cells were evaluated using Cell Counting Kit-8, apoptosis, and 5-ethynyl-2'-deoxyuridine assays. Target genes were identified via ribonucleic acid pull-down and luciferase reporter assays.ResultsHerein, micro ribonucleic acid-154-5p levels were upregulated in intracranial aneurysms. Furthermore, micro ribonucleic acid-154-5p promotes the intracranial aneurysm phenotype in vascular smooth muscle cells. H2O2-exposed vascular smooth muscle cells secrete exosomal micro ribonucleic acid-154-5p, which can be transferred to other vascular smooth muscle cells. Exosomal micro ribonucleic acid-154-5p promotes the development of intracranial aneurysms phenotype in vascular smooth muscle cells by targeting myosin light chain kinase.ConclusionsExosomal micro ribonucleic acid-154-5p is a novel potentially associated and promising therapeutic target for intracranial aneurysm management. However, the current study is limited to in vitro evidence.