1. Academic Validation
  2. Different origins of lysophospholipid mediators between coronary and peripheral arteries in acute coronary syndrome

Different origins of lysophospholipid mediators between coronary and peripheral arteries in acute coronary syndrome

  • J Lipid Res. 2017 Feb;58(2):433-442. doi: 10.1194/jlr.P071803.
Makoto Kurano 1 2 Kuniyuki Kano 2 3 Tomotaka Dohi 4 Hirotaka Matsumoto 3 Koji Igarashi 5 Masako Nishikawa 1 2 Ryunosuke Ohkawa 6 Hitoshi Ikeda 1 2 6 Katsumi Miyauchi 4 Hiroyuki Daida 4 Junken Aoki 2 3 Yutaka Yatomi 7 2 6
Affiliations

Affiliations

  • 1 Department of Clinical Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.
  • 2 CREST, Japan Science and Technology Corporation (JST).
  • 3 Laboratory of Molecular and Cellular Biochemistry, Graduate School of Pharmaceutical Sciences, Tohoku University, Miyagi, Japan.
  • 4 Department of Cardiovascular Medicine, Juntendo University School of Medicine, Tokyo, Japan.
  • 5 Bioscience Division, Reagent Development Department, AIA Research Group, TOSOH Corporation, Kanagawa, Japan.
  • 6 Department of Clinical Laboratory, University of Tokyo Hospital, Tokyo, Japan.
  • 7 Department of Clinical Laboratory Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan yatoyuta-tky@umin.ac.jp.
Abstract

Lysophosphatidic acids (LysoPAs) and lysophosphatidylserine (LysoPS) are emerging lipid mediators proposed to be involved in the pathogenesis of acute coronary syndrome (ACS). In this study, we attempted to elucidate how LysoPA and LysoPS become elevated in ACS using human blood samples collected simultaneously from culprit coronary arteries and peripheral arteries in ACS subjects. We found that: 1) the plasma LysoPA, LysoPS, and lysophosphatidylglycerol levels were not different, while the lysophosphatidylcholine (LysoPC), lysophosphatidylinositol, and lysophosphatidylethanolamine (LysoPE) levels were significantly lower in the culprit coronary arteries; 2) the serum Autotaxin (ATX) level was lower and the serum phosphatidylserine-specific Phospholipase A1 (PS-PLA1) level was higher in the culprit coronary arteries; 3) the LysoPE and ATX levels were significant explanatory factors for the mainly elevated species of LysoPA, except for 22:6 LysoPA, in the peripheral arteries, while the LysoPC and LysoPE levels, but not the ATX level, were explanatory factors in the culprit coronary arteries; and 4) 18:0 and 18:1 LysoPS were significantly correlated with PS-PLA1 only in the culprit coronary arteries. In conclusion, the origins of LysoPA and LysoPS might differ between culprit coronary arteries and peripheral arteries, and substrates for ATX, such as LysoPC and LysoPE, might be important for the generation of LysoPA in ACS.

Keywords

acute coronary disease; lysophosphatidic acids; lysophosphatidylcholine; lysophosphatidylethanolamine; lysophosphatidylserine.

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