Abstract
Oxidized LDL (oxLDL) is a known risk factor for atherogenesis. This study aimed to reveal structural features of oxLDL present in human circulation related to atherosclerosis. When LDL was fractionated on an anion-exchange column, in vivo-oxLDL, detected by the anti-oxidized PC (oxPC) mAb, was recovered in flow-through and electronegative LDL [LDL(-)] fractions. The amount of the electronegative in vivo-oxLDL, namely oxLDL in the LDL(-) fraction, present in patients with acute MI was 3-fold higher than that observed in healthy subjects. Surprisingly, the LDL(-) fraction contained apoA1 in addition to apoB, and HDL-sized particles were observed with transmission electron microscopy. In LDL(-) fractions, acrolein adducts were identified at all lysine residues in apoA1, with only a small number of acrolein-modified residues identified in apoB. The amount of oxPC adducts of apoB was higher in the LDL(-) than in the L1 fraction, as determined using Western blotting. The electronegative in vivo-oxLDL was immunologically purified from the LDL(-) fraction with an anti-oxPC mAb. The majority of PC species were not oxidized, whereas oxPC and lysoPC did not accumulate. Here, we propose that there are two types of in vivo-oxLDL in human circulating plasma and the electronegative in vivo-oxLDL accompanies oxidized HDL.
Highlights
Oxidized LDL is a known risk factor for atherogenesis
ApoB was detected in all four peaks and Oxidized LDL (oxLDL) was detected mostly in the flow-through fraction of LDL from anion-exchange column (L1) and LDL( ) fractions when the elution profiles of apoB and oxLDL were examined by sandwich ELISA (Fig. 1A, B)
The oxLDL/apoB ratios of the LDL( ) fraction in acute MI (AMI) patients and healthy controls were 3- and 6-fold higher than those observed in the L1 fraction, respectively
Summary
Oxidized LDL (oxLDL) is a known risk factor for atherogenesis. This study aimed to reveal structural features of oxLDL present in human circulation related to atherosclerosis. The amount of the electronegative in vivo-oxLDL, namely oxLDL in the LDL( ) fraction, present in patients with acute MI was 3-fold higher than that observed in healthy subjects. The electronegative in vivo-oxLDL was immunologically purified from the LDL( ) fraction with an anti-oxPC mAb. The majority of PC species were not oxidized, whereas oxPC and lysoPC did not accumulate. In human coronary arteries and carotid arteries, the accumulation of oxLDL in foam cells has been verified in previous studies [9, 10]. These results provide convincing evidence that oxLDL is present in atherosclerotic lesions
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