Circ_0000006 and circ_0000160 regulate hsa-let-7e-5p/UBQLN4 axis in aortic dissection progression.

Circ_0000006 and circ_0000160 regulate hsa-let-7e-5p/UBQLN4 axis in aortic dissection progression.

Blog Article

Aortic aneurysms (AA) and aorta dissection (AD) are life-threatening conditions with a rising incidence and high mortality rate.Recent research has linked non-coding RNAs to the regulation of AA and AD progression.In this study, we performed circRNA sequencing, microRNA (miRNA) sequencing, koleston 55/44 and messenger RNA (mRNA) sequencing on plasma samples from AA and AD patients to identify the key circRNA-miRNA-mRNA axis involved in the transition from AA to AD.Our results showed elevated levels of circ_0000006 and circ_0000160, along with decreased levels of hsa-let-7e-5p in AD samples compared to AA samples.

Predictive analysis suggested that circ_0000006 and circ_0000160 potentially target hsa-let-7e-5p, which in turn may bind to the mRNA of Ubiquilin 4 (UBQLN4).In an AD cell model using vascular smooth muscle cells (VSMCs), silencing circ_0000006 and circ_0000160 attenuated the effects of platelet-derived growth factor (PDGF)-induced phenotypic changes, proliferation, and migration.This effect was partially reversed by inhibiting hsa-let-7e-5p.Furthermore, we found that overexpression of UBQLN4 counteracted the effects of hsa-let-7e-5p, suggesting UBQLN4 as a downstream mediator of hsa-let-7e-5p.

In an animal model of AD, knockdown of circ_0000006 and circ_0000160 also showed protective effects against aortic septation.Overall, our findings indicate that the upregulation bible flask of circ_0000006 and circ_0000160 contributes to the progression from AA to AD by influencing abnormal phenotypic changes, migration, and proliferation of VSMCs.The Hsa-let-7e-5p/UBQLN4 axis may play a critical role in AD development.Targeting circ_0000006 and circ_0000160 could be a potential therapeutic strategy for preventing the progression of AD.