MicroRNA-155 promotes neointimal hyperplasia through smooth muscle-like cell-derived RANTES in arteriovenous fistulas.

Abstract

OBJECTIVE:

Arteriovenous fistula (AVF) suffers from a high number of failures caused by insufficient outward remodeling and venous neointimal hyperplasia formation. The aim was to investigate the exact mechanism by which microRNA-155 (miR-155) in the outflow vein of AVF is regulated.

METHODS:

AVFs between the branch of the jugular vein and carotid artery in an end-to-end manner were created in C57BL/6 and miR-155-/- mice with a C57BL/6 background. The venous segments were harvested at day 7, 14, 21, and 28, and the AVFs were analyzed histologically and at a messenger RNA level using real-time quantitative polymerase chain reactions. The outflow vein of AVF and the normal great saphenous vein, collected from patients with chronic kidney disease and coronary artery bypass surgery, were analyzed by histologic and molecular biologic approaches.

RESULTS:

Venous neointimal hyperplasia is significantly alleviated in miR-155-/- mice, and the expression of several chemokines and cytokines in the vessel wall, including regulated on activation, normal T-cell expressed and secreted factor (RANTES), monocyte chemoattractant protein 1, and vascular endothelial growth factor, was inhibited. miR-155 promoted the RANTES expression of smooth muscle-like cells, which in turn facilitated cell proliferation and extracellular matrix production.

CONCLUSIONS:

miR-155 enhances venous neointima formation through the autocrine and paracrine effects of smooth muscle-like cell-derived RANTES in a nuclear factor κB-dependent manner during the entire AVF process, especially at the advanced stage.

• Authors: Ke Wang, Peng Deng, Yuan Sun, Ping Ye, Anchen Zhang, Chuangyan Wu, Zhang Yue, Zhaolei Chen, Jiahong Xia
• Journal: Journal of vascular surgery (J Vasc Surg) Vol. 67 Issue 3 Pg. 933-944.e3 (03 2018) ISSN: 1097-6809 [Electronic] United States
• PMID: 29477204 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2017. Published by Elsevier Inc.

Chemical References

• CCL5 protein, human
• Ccl5 protein, mouse
• Chemokine CCL5
• Inflammation Mediators
• MIRN155 microRNA, human
• MicroRNAs
• Mirn155 microRNA, mouse
• NF-kappa B
• RNA, Messenger

Topics

• Animals
• Arteriovenous Shunt, Surgical (adverse effects)
• Autocrine Communication
• Cell Proliferation
• Chemokine CCL5 (genetics, metabolism)
• Humans
• Hyperplasia
• Inflammation Mediators (metabolism)
• Mice, Inbred C57BL
• Mice, Knockout
• MicroRNAs (genetics, metabolism)
• Muscle, Smooth, Vascular (metabolism, pathology)
• Myocytes, Smooth Muscle (metabolism, pathology)
• NF-kappa B (metabolism)
• Neointima
• Paracrine Communication
• RNA, Messenger (genetics, metabolism)
• Signal Transduction
• Time Factors