Please use this identifier to cite or link to this item:
Title: Aorta macrophage inflammatory and epigenetic changes in a murine model of obstructive sleep apnea: Potential role of CD36
Author: Cortese, Rene
Gileles-Hillel, Alex
Khalyfa, Abdelnaby
Almendros López, Isaac
Akbarpour, Mahzad
Khalyfa, Khalyfa, Ahamed A.
Qiao, Zhuanhong
Garcia, Tzintzuni
Andrade, Jorge
Gozal, David
Keywords: Síndromes d'apnea del son
Oxigen en l'organisme
Malalties cardiovasculars
Sleep apnea syndromes
Oxygen in the body
Cardiovascular diseases
Issue Date: 27-Feb-2017
Publisher: Nature Publishing Group
Abstract: Obstructive sleep apnea (OSA) affects 8-10% of the population, is characterized by chronic intermittent hypoxia (CIH), and causally associates with cardiovascular morbidities. In CIH-exposed mice, closely mimicking the chronicity of human OSA, increased accumulation and proliferation of pro-inflammatory metabolic M1-like macrophages highly expressing CD36, emerged in aorta. Transcriptomic and MeDIP-seq approaches identified activation of pro-atherogenic pathways involving a complex interplay of histone modifications in functionally-relevant biological pathways, such as inflammation and oxidative stress in aorta macrophages. Discontinuation of CIH did not elicit significant improvements in aorta wall macrophage phenotype. However, CIH-induced aorta changes were absent in CD36 knockout mice, Our results provide mechanistic insights showing that CIH exposures during sleep in absence of concurrent pro-atherogenic settings (i.e., genetic propensity or dietary manipulation) lead to the recruitment of CD36(+)high macrophages to the aortic wall and trigger atherogenesis. Furthermore, long-term CIH-induced changes may not be reversible with usual OSA treatment.
Note: Reproducció del document publicat a:
It is part of: Scientific Reports, 2017, vol. 7, p. 43648
Related resource:
ISSN: 2045-2322
Appears in Collections:Articles publicats en revistes (Biomedicina)

Files in This Item:
File Description SizeFormat 
678321.pdf1.81 MBAdobe PDFView/Open

This item is licensed under a Creative Commons License Creative Commons