What question did this study set out to answer?

To determine whether enzymatic modification of human low density lipoprotein generates atherogenic particles equivalent to lipids isolated from atherosclerotic plaques.

December 1, 1995The Journal of Experimental MedicineOpen Access

On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.

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Authors

SBS BhakdiJohannes Gutenberg University Mainz BDBernhard DorweilerUniversity of Cologne RKR. KirchmannUniversity of Liège

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Implication

In vitro study demonstrates triple enzyme treatment transforms human low-density lipoprotein into complement-activating atherogenic particles, suggesting an enzymatic trigger for atherosclerosis.

Key Points

To determine whether enzymatic modification of human low density lipoprotein generates atherogenic particles equivalent to lipids isolated from atherosclerotic plaques.
Treated human LDL, HDL, and VLDL with single, double, or triple combinations of trypsin, cholesterol esterase, and neuraminidase, comparing results against phospholipase C or vortexing.
Assessed particle morphology, oxidation status, complement cascade activation pathways, and uptake rates in cultured human macrophages via competition assays.
Triple enzyme treatment transformed LDL into negatively charged lipid droplets (10–200 nm) lacking oxidation that fully activated complement through the alternative pathway.
E-LDL induced cholesteryl oleate ester formation in macrophages at 6–10 nmol/mg protein compared with 3–6 nmol/mg for acetylated LDL without causing direct cytotoxicity.
A 2-fold excess of unlabeled E-LDL inhibited approximately 90% of 125I-ox-LDL degradation, indicating uptake is partially mediated by ox-LDL receptors.

Cite This Study

Bhakdi et al. (1995) studied this question.

synapsesocial.com/papers/6a6dfb0fce524a4339c2dc98 https://doi.org/10.1084/jem.182.6.1959

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Implication

In vitro study demonstrates triple enzyme treatment transforms human low-density lipoprotein into complement-activating atherogenic particles, suggesting an enzymatic trigger for atherosclerosis.

On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.

Discussion

Member takes

Implication

Key Points

Cite This Study

On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.

Discussion

Member takes

Implication

Key Points

Cite This Study

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