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Research Article

Migration of OxLDL+ Macrophage Phenotypes from Pericoronary Adipose Tissue to Coronary Intima: A Possible Mechanism for Human Coronary Atherosclerosis

Author: Yasumi Uchida1, Yasuto Uchida, Ei Shimoyama, Nobuyuki Hiruta and Tsuyoshi Tabata

Published Online: March 30, 2021

DOI: 10.34297/AJBSR.2021.12.001750.


Background: We previously found that oxidized low-density lipoprotein (oxLDL), a core atherogenic protein, is stored in human pericoronary adipose tissue (PCAT) and macrophages residing in PCAT accumulate oxLDL. Here, we aimed to identify whether and how the macrophage phenotypes transport oxLDL from PCAT to the coronary intima. Methods and results: Coronary arteries and their surrounding PCAT were excised from human autopsy subjects and examined using immunohistochemical techniques to investigate macrophage-mediated oxLDL transport from PCAT to the coronary intima. OxLDL+CD68+ and oxLDL+CD206+ macrophages were observed in PCAT of both normal coronary segments (normal group) and adjacent coronary segments with plaques (plaque group). External elastic lamina (EEL) was loosened, or fragmented and internal elastic lamina (IEL) was disrupted in the plaque group, and oxLDL+CD68+ and oxLDL+C206+ macrophages extending pseudopod forward were frequently observed to pass through these portions into the intima. OxLDL+CD11c+ macrophages were not found in PCAT, EEL and the media but were found in disrupted IEL and plaques. Conclusions: The results suggest that CD206+ or CD68+ macrophages transport oxLDL from PCAT into the media and they and CD11c+ macrophages transformed at the site of IEE into plaque via loosened or fragmented EEL and disrupted IEL and could participate in initiation and acceleration of human coronary atherosclerosis. Keywords: Human coronary plaques, Immunohistochemical staining, Macrophage phenotypes, Oxidized low-density lipoprotein, Pericoronary adipose tissue Introduction

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