{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T22:53:32Z","timestamp":1790808812521,"version":"4.1.0"},"reference-count":54,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2023,8,21]],"date-time":"2023-08-21T00:00:00Z","timestamp":1692576000000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical &amp; Translational Med"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Cardiovascular diseases (CVDs) prevalence has significantly increased in the last decade and atherosclerosis development is the main trigger. MicroRNAs (miRNAs) are non\u2010coding RNAs that negatively regulate gene expression of their target and their levels are frequently altered in CVDs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>By RT\u2010qPCR, we analysed miR\u20109\u20105p, miR\u201015a\u20105p, miR\u201016\u20105p and miR\u2010199a\u20103p levels in aorta from apolipoprotein knockout (<jats:italic>ApoE<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic>) mice, an experimental model of hyperlipidemia\u2010induced atherosclerosis, and in human aortic and carotid atherosclerotic samples. By in silico studies, Western blot analysis and immunofluorescence studies, we detected the targets of the altered miRNAs.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Our results show that miR\u201015a\u20105p and miR\u2010199a\u20103p are significantly decreased in carotid and aortic samples from patients and mice with atherosclerosis. In addition, we found an increased expression in targets of both miRNAs that participate in the inflammatory pathway of nuclear factor kappa B (NF\u2010\u03baB), such as IKK\u03b1, IKK\u03b2 and p65. In human vein endothelial cells (HUVECs) and vascular smooth muscle cells (VSMCs), the overexpression of miR\u201015a\u20105p or miR\u2010199a\u20103p decreased IKK\u03b1, IKK\u03b2 and p65 protein levels as well as NF\u2010\u03baB activation. On the other hand, miR\u201015a\u20105p and miR\u2010199a\u20103p overexpression reduced ox\u2010LDL uptake and the inflammation regulated by NF\u2010\u03baB in VSMCs. Moreover, although miR\u201015a\u20105p and miR\u2010199a\u20103p were significantly increased in exosomes from patients with advanced carotid atherosclerosis, only in the ROC analyses for miR\u201015a\u20105p, the area under the curve was 0.8951 with a <jats:italic>p<\/jats:italic> value of .0028.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Our results suggest that the decrease of miR\u2010199a\u20103p and miR\u201015a\u20105p in vascular samples from human and experimental atherosclerosis could be involved in the NF\u2010\u03baB activation pathway, as well as in ox\u2010LDL uptake by VSMCs, contributing to inflammation and progression atherosclerosis. Finally, miR\u201015a\u20105p could be used as a novel diagnostic biomarker for advanced atherosclerosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ctm2.1363","type":"journal-article","created":{"date-parts":[[2023,8,22]],"date-time":"2023-08-22T06:09:57Z","timestamp":1692684597000},"source":"Crossref","is-referenced-by-count":49,"title":["Role of miR\u201015a\u20105p and miR\u2010199a\u20103p in the inflammatory pathway regulated by NF\u2010\u03baB in experimental and human atherosclerosis"],"prefix":"10.1002","volume":"13","author":[{"given":"Paula","family":"Gonz\u00e1lez\u2010L\u00f3pez","sequence":"first","affiliation":[{"name":"Hepatic and Vascular Diseases Laboratory. Biochemistry and Molecular Biology Department, School of Pharmacy Complutense University of Madrid  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marta","family":"\u00c1lvarez\u2010Villarreal","sequence":"additional","affiliation":[{"name":"Hepatic and Vascular Diseases Laboratory. Biochemistry and Molecular Biology Department, School of Pharmacy Complutense University of Madrid  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rub\u00e9n","family":"Ruiz\u2010Sim\u00f3n","sequence":"additional","affiliation":[{"name":"Hepatic and Vascular Diseases Laboratory. Biochemistry and Molecular Biology Department, School of Pharmacy Complutense University of Madrid  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea R.","family":"L\u00f3pez\u2010Pastor","sequence":"additional","affiliation":[{"name":"Hepatic and Vascular Diseases Laboratory. Biochemistry and Molecular Biology Department, School of Pharmacy Complutense University of Madrid  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Melina Vega","family":"de Ceniga","sequence":"additional","affiliation":[{"name":"Department of Angiology and Vascular Surgery Hospital of Galdakao\u2010Usansolo  Galdakao Bizkaia Spain"},{"name":"Biocruces Bizkaia Health Research Institute  Barakaldo Bizkaia Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leticia","family":"Esparza","sequence":"additional","affiliation":[{"name":"Department of Angiology and Vascular Surgery Hospital of Galdakao\u2010Usansolo  Galdakao Bizkaia Spain"},{"name":"Biocruces Bizkaia Health Research Institute  Barakaldo Bizkaia Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e9 L.","family":"Mart\u00edn\u2010Ventura","sequence":"additional","affiliation":[{"name":"IIS\u2010Fundation Jimenez\u2010Diaz Autonoma University of Madrid and CIBERCV  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8249-1645","authenticated-orcid":false,"given":"\u00d3scar","family":"Escribano","sequence":"additional","affiliation":[{"name":"Hepatic and Vascular Diseases Laboratory. 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