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Am J Physiol Heart Circ Physiol (March 14, 2002). doi:10.1152/ajpheart.00524.2001
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Articles in PresS, published online ahead of print March 14, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00524.2001
Submitted on June 15, 2001
Accepted on February 19, 2002

Increasing plasmalogen levels protects human endothelial cells during hypoxia

Raphael A. Zoeller1*, Todd J. Grazia2, Peter LaCamera2, James Park2, Daniel P. Gaposchkin1, and Harrison W. Farber2

1 Department of Physiology and Biophysics, Boston University School of Medicine, Boston, MA, USA
2 The Pulmonary Center, Boston University School of Medicine, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: rzoeller{at}bu.edu.

Supplementation of cultured human pulmonary arterial endothelial cells (HPAEC) with sn-1-O-hexadecylglycerol (HG) resulted in an approximately 2-fold increase in the cellular levels of plasmalogens, a subclass of phospholipids known to have antioxidant properties; this was due, primarily, to a 4 fold-increase in the choline plasmalogens. Exposure of unsupplemented HPAEC to hypoxia (pO2 = 20-25 mm Hg) caused an increase in cellular reactive oxygen species (ROS) over a period of 5 days, with a coincident decrease in viability. In contrast, HG-supplemented cells survived under these conditions with no evidence of increased ROS. Hypoxia resulted in a selective increase in the turnover of the plasmalogen, plasmenylethanolamine. This protection was seemingly specific to cellular stresses in which significant ROS were generated. HPAEC with elevated plasmalogen levels were also more resistant to H2O2, hyperoxia, and the superoxide generator plumbagin. This is the initial demonstration that plasmalogen content can be enhanced in a normal cell and suggests that these phospholipids play a significant role in cellular protection during hypoxia, possibly due to their antioxidant properties.




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