| Autor: |
Carpenter KL; Department of Pathology, University of Cambridge, UK. klhc@mole.bio.cam.ac.uk, Dennis IF, Challis IR, Osborn DP, Macphee CH, Leake DS, Arends MJ, Mitchinson MJ |
| Jazyk: |
angličtina |
| Zdroj: |
FEBS letters [FEBS Lett] 2001 Sep 21; Vol. 505 (3), pp. 357-63. |
| DOI: |
10.1016/s0014-5793(01)02840-x |
| Abstrakt: |
The death of macrophages contributes to atheroma formation. Oxidation renders low-density lipoprotein (LDL) cytotoxic to human monocyte-macrophages. Lipoprotein-associated phospholipase A2 (Lp-PLA2), also termed platelet-activating factor acetylhydrolase, hydrolyses oxidised phospholipids. Inhibition of Lp-PLA2 by diisopropyl fluorophosphate or Pefabloc (broad-spectrum serine esterase/protease inhibitors), or SB222657 (a specific inhibitor of Lp-PLA2) did not prevent LDL oxidation, but diminished the ensuing toxicity and apoptosis induction when the LDL was oxidised, and inhibited the rise in lysophosphatidylcholine levels that occurred in the inhibitors' absence. Hydrolysis products of oxidised phospholipids thus account for over a third of the cytotoxic and apoptosis-inducing effects of oxidised LDL on macrophages. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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