WITHDRAWN: Atf1-activated Tgfbr2 promotes abdominal aortic aneurysm by snhg1/miR-211-5p/Tgfbr2 axis

Abstract

<h2>Abstract</h2><h3>Objective</h3> To explore the role of Snhg1/miR-211-5p/Tgfbr2 axis in Abdominal aortic aneurysm (AAA). <h3>Design</h3> AAA features dilated abdominal aorta 50% greater than normal aorta, and in some cases aorta can grow more than 28 mm in diameter. AAA is a prominent reason for sudden death among elder people. <h3>Setting</h3> All the assays were conducted in central laboratory of Wuhan Union Hospital. <h3>Participants</h3> The study was accomplished by Wuhan Union Hospital. <h3>Interventions</h3> Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot were implemented to evaluate RNA and protein levels. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and flow cytometry assays were performed to evaluate apoptosis of AAA cells. Dual-luciferase reporter, RNA pull down, and chromatin immunoprecipitation (ChIP) assays were carried out to evaluate the underlying mechanisms. <h3>Measurements & Main Results</h3> The p-value cutoff was set as 0.05 for statistical significance. Experimental results were presented as the mean value ± standard deviation. Inhibited Tgfbr2 could reduce the apoptosis and extracellular matrix disruption of vascular smooth muscle cell. MiR-211-5p could bind to Tgfbr2 and Snhg1, and inhibited Snhg1 to suppress AAA. Atf1 activated the expression of Snhg1. Snhg1/miR-211-5p/Tgfbr2 axis played an important regulatory role in vascular smooth muscle cells. <h3>Conclusions</h3> Atf1-activated Tgfbr2 promotes abdominal aortic aneurysm by snhg1/miR-211-5p/Tgfbr2 axis.