MicroRNA-24 attenuates diabetic vascular remodeling by suppressing the NLRP3/caspase-1/IL-1β signaling pathway

Vascular remodeling plays an important role in the pathogenesis of diabetic cardiovascular complications. Previous published research has indicated that microRNA-24 (miR-24) is involved in diabetic vascular remodeling, but the underlying molecular mechanisms have yet to be fully elucidated. The aim of the present study was to investigate whether adenovirus-mediated miR-24 overexpression can suppress the NOD-like receptor family pyrin domain-containing 3 (NLRP3)-related inflammatory signaling pathway and attenuate diabetic vascular remodeling. The carotid arteries of diabetic rats were harvested and prepared for analysis. Reverse transcription-quantitative PCR and western blotting assays were used to detect the expressions of related mRNAs and proteins. Morphological examinations, including hematoxylin and eosin, immunohistochemical and Masson's trichrome staining, were also performed. The results of the present study demonstrated that miR-24 upregulation suppressed neointimal hyperplasia and accelerated reendothelialization in the injured arteries, lowered the expression of NLRP3, apoptosis-associated speck-like protein, caspase-1, proliferating cell nuclear antigen, CD45, interleukin (IL)-1 beta, IL-18 and tumor necrosis factor-alpha, and increased the expression of CD31, smooth muscle (SM) alpha -actin and SM-myosin heavy chain. These data indicated that miR-24 overexpression can attenuate vascular remodeling in a diabetic rat model through suppressing the NLRP3/caspase-1/IL-1 beta signaling pathway.