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Poster Abstract PresentationsSession Title: Poster Session III

Abstract 451: HPODE Upregulates the Expression of Secretory Phospholipase A2 Group IIA in Rat Smooth Muscle Cells. Potential Contribution to the Progression of Atherosclerosis

Zhaohui Yang, Chandrakala Aluganti Narasimhulu, Xueting Jiang, Sampath Parthasarathy
Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;32:A451
Zhaohui Yang
Burnett Sch of Biomedical Sciences, Univ of Central Florida, Orlando, FL
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Chandrakala Aluganti Narasimhulu
Burnett Sch of Biomedical Sciences, Univ of Central Florida, Orlando, FL
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Xueting Jiang
Burnett Sch of Biomedical Sciences, Univ of Central Florida, Orlando, FL
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Sampath Parthasarathy
Burnett Sch of Biomedical Sciences, Univ of Central Florida, Orlando, FL
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Abstract

Introduction Peroxidized lipids have been suggested to contribute to atherosclerosis in a number of ways. Accumulating evidence indicates that Group IIA secretory phospholipase A2 (sPLA2-IIA) may contribute to the atherogenic process and serve as markers for cardiovascular diseases. However, the relationship between lipid peroxides and sPLA2-IIA remain poorly identified.

Hypothesis Peroxidized lipids such as HPODEs might induce the expression of sPLA2-IIA and enhance the uptake of LDL, thereby contributing to lipid accumulation.

Methods Different concentrations of HPODE (0 μM, 12.5μM, 25μM) or oxidized -LDL (ox-LDL) (25μg/ml) were incubated with SMCs at 37°C. Real-time PCR was used to assay gene expression. The degradation of HPODE and ox-LDL was also monitored by the loss of peroxides and conjugated dienes. The formation of HPODE decomposition products was followed by electrospray mass spectrometry.

Results Incubation of SMCs with HPODE resulted in an up-regulation of sPLA2-IIA mRNA expression in a concentration dependent manner. However, ox-LDL had limited or no effects in the expression of sPLA2. In addition, SMCs and peritoneal mouse macrophages pretreated with HPODE for 8hrs followed by DiI-LDL (20μg/ml) showed an increase in accumulation of labeled LDL as compared to control. We also noted that HPODE was decomposed by SMCs in hours as compared to no cell incubations. However, incubation of peroxidized lipids in the form of ox-LDL resulted in poor decomposition of the peroxides.

Conclusion SMCs may break down the peroxidized fatty acids leading to the formation of simple compounds such as aldehydes and carboxylic acids. HPODE or its decomposition products may induce the expression of sPLA2-II and enhance foam cell formation.

  • smooth muscle cells
  • sPLA2
  • oxidized -LDL
  • © 2012 by American Heart Association, Inc.
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    Abstract 451: HPODE Upregulates the Expression of Secretory Phospholipase A2 Group IIA in Rat Smooth Muscle Cells. Potential Contribution to the Progression of Atherosclerosis
    Zhaohui Yang, Chandrakala Aluganti Narasimhulu, Xueting Jiang and Sampath Parthasarathy
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;32:A451, originally published October 20, 2015

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    Abstract 451: HPODE Upregulates the Expression of Secretory Phospholipase A2 Group IIA in Rat Smooth Muscle Cells. Potential Contribution to the Progression of Atherosclerosis
    Zhaohui Yang, Chandrakala Aluganti Narasimhulu, Xueting Jiang and Sampath Parthasarathy
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2012;32:A451, originally published October 20, 2015
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