González-López, PaulaAres-Carral, CarlaLópez-Pastor, Andrea R.Infante-Menéndez, JorgeGonzález Illanes, TamaraVega de Ceniga, MelinaEsparza, LeticiaBeneit, NuriaMartín-Ventura, José LuisEscribano Illanes, ÓscarGómez Hernández, María De La Almudena2024-01-172024-01-172022-09-06González-López P, Ares-Carral C, López-Pastor AR, Infante-Menéndez J, González Illaness T, Vega De Ceniga M, et al. Implication of miR-155-5p and miR-143-3p in the Vascular Insulin Resistance and Instability of Human and Experimental Atherosclerotic Plaque. IJMS 2022;23:10253. https://doi.org/10.3390/ijms231810253.1661-659610.3390/ijms231810253https://hdl.handle.net/20.500.14352/93718(1) Background: Cardiovascular diseases (CVDs) are the main cause of death in developed countries, being atherosclerosis, a recurring process underlying their apparition. MicroRNAs (miRNAs) modulate the expression of their targets and have emerged as key players in CVDs; (2) Methods: 18 miRNAs were selected (Pubmed and GEO database) for their possible role in promoting atherosclerosis and were analysed by RT-qPCR in the aorta from apolipoprotein E-deficient (ApoE−/−) mice. Afterwards, the altered miRNAs in the aorta from 18 weeks-ApoE−/− mice were studied in human aortic and carotid samples; (3) Results: miR-155-5p was overexpressed and miR-143-3p was downregulated in mouse and human atherosclerotic lesions. In addition, a significant decrease in protein kinase B (AKT), target of miR-155-5p, and an increase in insulin-like growth factor type II receptor (IGF-IIR), target of miR-143-3p, were noted in aortic roots from ApoE−/− mice and in carotid plaques from patients with advanced carotid atherosclerosis (ACA). Finally, the overexpression of miR-155-5p reduced AKT levels and its phosphorylation in vascular smooth muscle cells, while miR-143-3p overexpression decreased IGF-IIR reducing apoptosis in vascular cells; (4) Conclusions: Our results suggest that miR-155-5p and miR-143-3p may be implicated in insulin resistance and plaque instability by the modulation of their targets AKT and IGF-IIR, contributing to the progression of atherosclerosis.engAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/journal article1422-0067https://doi.org/10.3390/ijms231810253open access577.2atherosclerosismiR-155-5pmiR-143-3punstable plaqueapoptosisAKTIGF-IIRBiología molecular (Farmacia)Bioquímica (Farmacia)2302 Bioquímica2415 Biología Molecular