Aorta macrophage inflammatory and epigenetic changes in a murine model of obstructive sleep apnea: Potential role of CD36

• DOI: 10.1038/srep43648
• Publication Date: 2017-02-27T10:34:07Z
• Authors: Rene Cortese; Alex Gileles-Hillel; Abdelnaby Khalyfa; Isaac Almendros; Mahzad Akbarpour; Ahamed A. Khalyfa; Zhuanghong Qiao; Tzintzuni Garcia; Jorge Andrade; David Gozal
• Keywords: CD36

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 chronicity human OSA, increased accumulation proliferation pro-inflammatory metabolic M1-like macrophages highly expressing CD36, emerged in aorta. Transcriptomic MeDIP-seq approaches identified activation pro-atherogenic pathways involving a complex interplay histone modifications functionally-relevant biological pathways, such as inflammation oxidative stress aorta macrophages. Discontinuation CIH did not elicit significant improvements wall macrophage phenotype. However, CIH-induced changes were absent CD36 knockout Our results provide mechanistic insights showing that exposures during absence concurrent settings (i.e., genetic propensity or dietary manipulation) lead to recruitment CD36(+) high aortic trigger atherogenesis. Furthermore, long-term may be reversible usual OSA treatment.