Nonhematopoietic MicroRNA-26b −/− Augments Atherosclerosis Development by Increasing Endothelial Inflammation and Leukocyte Adhesion—Brief Report

Peters, Linsey J.F.; Bidzhekov, Kiril; Megens, Remco T.A. ; Jansen, Yvonne; Jin, Han; Jans, Alexander; Lin, Cheng ; Haberbosch, Markus ; Bartneck, Matthias ; Biessen, Erik A.L. ; Weber, Christian ; Döring, Yvonne und Vorst, Emiel P.C. van der (2026): Nonhematopoietic MicroRNA-26b −/− Augments Atherosclerosis Development by Increasing Endothelial Inflammation and Leukocyte Adhesion—Brief Report. In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 46, No. 3, e323888

Abstract

BACKGROUND: Atherosclerosis is a leading cause of cardiovascular diseases, and microRNA-26b (miR-26b) has emerged as a significant regulator in its development. This study investigates the role of nonhematopoietic miR-26b in atherosclerosis. METHODS: To study the specific role of nonhematopoietic cell miR-26b in atherosclerosis development, we used a reverse bone marrow transplantation model combined with 12-week Western-type diet feeding. RESULTS: Nonhematopoietic-specific miR-26b deficiency exacerbated atherosclerosis, characterized by larger plaques with increased collagen and necrotic core content. Enhanced VCAM-1 (vascular cell adhesion molecule 1) expression correlated with elevated leukocyte adhesion in ex vivo perfusion studies. Restoration of miR-26b levels in human coronary artery endothelial cells reduced inflammatory responses and leukocyte adhesion. CONCLUSIONS: Our findings highlight that nonhematopoietic miR-26b plays a protective role in atherosclerosis by modulating endothelial cell function, suggesting potential therapeutic applications for miR-26b mimics in cardiovascular disease management.

• Item Type: Journal article
• Faculties: Medicine > Munich Cluster for Systems Neurology (SyNergy); Medicine > Medical Center of the University of Munich > Institute for Cardiovascular Prevention (IPEK)
• Subjects: 600 Technology > 610 Medicine and health
• ISSN: 1079-5642
• Language: English
• DFG: Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 390857198