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Related Experiment Videos

Anoxia and reoxygenation of human endothelial cells decrease ceramide glucosyltransferase expression and activates

Hui Zhao1, Mendy Miller, Kristine Pfeiffer

  • 1Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|February 15, 2003
PubMed
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Oxidative stress in endothelial cells increases caspase activity, a key factor in cell death. This study reveals that decreased glucosylceramide synthase (GCS) expression contributes to this caspase activation.

Area of Science:

  • Endothelial cell biology
  • Cellular stress responses
  • Biochemistry

Background:

  • Endothelial oxidative stress can lead to cell activation and death through necrosis or apoptosis.
  • Understanding these mechanisms is crucial for developing therapeutics targeting endothelial cell function.
  • Cellular activation and death pathways are complex and involve multiple signaling cascades.

Purpose of the Study:

  • To investigate the role of oxidative stress in human umbilical vein endothelial cell (HUVEC) death.
  • To identify molecular mechanisms, particularly sphingolipid metabolism, involved in oxidative stress-induced endothelial cell apoptosis.
  • To explore the relationship between glucosylceramide synthase (GCS) and caspase activity.

Main Methods:

  • HUVECs were subjected to anoxia followed by reoxygenation to induce oxidative stress.

Related Experiment Videos

  • Caspase activity, ROCK-1 cleavage, and GCS expression (mRNA and protein) were measured.
  • Microarray analysis was performed to identify modulated genes.
  • Specific inhibitors of GCS (PDMP) and ceramide synthase (Fumonisin B1) were used to assess their impact on caspase activity.

    • Main Results:

    • Anoxia/reoxygenation increased HUVEC caspase activity and ROCK-1 cleavage in a time-dependent manner.
    • Microarray and subsequent validation confirmed a time-dependent decrease in GCS mRNA and protein expression under oxidative stress.
    • Inhibition of GCS mimicked the effect of oxidative stress by increasing caspase activity.
    • Inhibition of ceramide synthase attenuated caspase activity in stressed HUVECs.

    Conclusions:

    • Decreased glucosylceramide synthase (GCS) expression is a key event in oxidative stress-induced caspase activation in endothelial cells.
    • Alterations in sphingolipid metabolism, specifically involving GCS, play a significant role in endothelial cell death pathways.
    • These findings suggest GCS as a potential therapeutic target for managing endothelial dysfunction.