June O'Neil
Cleveland Clinic
35 Papers
633 Citations
June O'Neil is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Scavenger receptor & Apolipoprotein B. The author has an hindex of 24, co-authored 35 publications. Previous affiliations of June O'Neil include Cleveland Clinic Lerner Research Institute & Case Western Reserve University.
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Papers
Lipoprotein(a) is an independent risk factor for cardiovascular disease in hemodialysis patients.
Michael D. Cressman,Robert J. Heyka,Emil P. Paganini,June O'Neil,Christine Skibinski,Henry F. Hoff +5 more
TL;DR: Lp(a) is an independent risk factor for clinical events attributed to atherosclerotic cardiovascular disease in patients receiving chronic hemodialysis treatment of end-stage renal disease, and baseline serum total cholesterol, triglyceride, high density lipoprotein cholesterol, low density cholesterol, age, gender, race, or duration of hemodIALysis were unrelated to this risk in the prospective study.
299
Modification of low density lipoprotein with 4-hydroxynonenal induces uptake by macrophages.
Henry F. Hoff,June O'Neil,G M Chisolm rd,T. B. Cole,Oswald Quehenberger,H Esterbauer,G. Jurgens +6 more
TL;DR: Interaction of LDL with HNE formed during lipid peroxidation could be responsible for structural modifications leading to unregulated uptake of the lipoprotein by tissue macrophages, which could partially explain lipid loading or foam cell formation in atherosclerosis.
199
Lesion-derived low density lipoprotein and oxidized low density lipoprotein share a lability for aggregation, leading to enhanced macrophage degradation.
Henry F. Hoff,June O'Neil +1 more
TL;DR: It is demonstrated that A- LDL and Ox-LDL share properties additional to those previously reported, suggesting that oxidation may be a major mode of modification of LDL accumulating in atherosclerotic lesions.
171
Oxidation of low density lipoprotein leads to particle aggregation and altered macrophage recognition.
TL;DR: Results from cross-competition studies in MPM were consistent with uptake of soluble ox- LDL via both the scavenger receptor and another receptor on MPM, and uptake of the insoluble ox-LDL by an alternative mechanism.
141
Inactivation of lysosomal proteases by oxidized low density lipoprotein is partially responsible for its poor degradation by mouse peritoneal macrophages.
TL;DR: The reduced degradation of lipoproteins in MPM pretreated with ox-LDL could be due to direct inactivation of the lysosomal protease, cathepsin B.