Lymphocyte resistance to lysophosphatidylcholine mediated apoptosis in atherosclerosis

Naomi Zurgil, Elena Afrimzon, Yana Shafran, Ora Shovman, Boris Gilburd, Haim Brikman, Yehuda Shoenfeld, Mordechai Deutsch

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Objective: Apoptosis is being increasingly regarded as a key component in the development and progression of atherosclerosis. Since it has become apparent that the immune system plays a predominant role in mediating atherogenesis, there has been a growing recognition that the evaluation of lymphocyte apoptosis may contribute to understanding a persistent altered immune and inflammatory response. The aim of the present study was to evaluate the apoptotic effect of lysophosphatidylcholine (LPC) on peripheral blood lymphocytes (PBL) derived from unstable angina (UA) patients, as compared to healthy donors. Methods: PBL isolated from 27 healthy donors and 25 age matched UA patients were examined. Early apoptotic events induced by LPC in resting and phytohemagglutinin (PHA)-activated lymphocytes were evaluated by several apoptotic assays. The levels of intracellular reactive oxygen species (ROS) and the expression of apoptotic regulated proteins (Bcl-2 and Bax) were measured. Results: LPC was found to induce apoptosis in normal activated lymphocytes, in a dose- and time-dependent manner, in association with an increase in intracellular ROS. In UA patients, an exposure of PHA-activated PBL to LPC triggered neither an increase in ROS generation, nor in the apoptotic manifestations, and was associated with a significantly lower ratio of Bax/Bcl-2 expression. Conclusion: Our results indicate that PBL isolated from UA patients may be resistant to apoptosis induction by LPC, resulting from oxidative stress challenge and dysregulation of apoptosis-related protein expression.

Original languageEnglish
Pages (from-to)73-83
Number of pages11
Issue number1
StatePublished - Jan 2007

Bibliographical note

Funding Information:
This research was supported by the Horowitz Foundation and by Molecular Cytomics Ltd.


This research was supported by the Horowitz Foundation and by Molecular Cytomics Ltd.

FundersFunder number
Molecular Cytomics Ltd.
Horowitz Foundation for Social Policy


    • Apoptosis
    • Atherosclerosis
    • Leukocytes
    • Oxygen radicals
    • Signal transduction


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