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Related Experiment Video

Updated: Jun 19, 2026

Fluorescence-Based Measurements of Phosphatidylserine/Phosphatidylinositol 4-Phosphate Exchange Between Membranes

Fluorescence-Based Measurements of Phosphatidylserine/Phosphatidylinositol 4-Phosphate Exchange Between Membranes

Published on: March 14, 2021

Phospholipase D modulation by ceramide in senescence.

Lisa M Webb¹, Alan T Arnholt, Mark E Venable

¹Biology Department, Appalachian State University, Boone, NC 28608-2027, USA.

Molecular and Cellular Biochemistry

|October 27, 2009

Summary

Senescent cells exhibit reduced Phospholipase D (PLD) activity due to a defective membrane component. Ceramide, a sphingolipid, mediates this inhibition, impacting cellular regulation.

Area of Science:

Cellular senescence
Enzymology
Molecular biology

Background:

Phospholipase D (PLD) plays a role in cell division and its activity decreases in senescent cells.
Replicative senescence affects cellular functions, including PLD activity.

Purpose of the Study:

To investigate the cause of reduced Phospholipase D activity in senescent cells.
To identify the specific cellular component responsible for PLD dysfunction during senescence.

Main Methods:

Fractionation of cellular components from senescent and low-passage human cells.
Recombination experiments to assess PLD activation with different cell fractions.
Treatment with ceramide to evaluate its effect on PLD activity.

Main Results:

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Senescent cells displayed significantly lower PLD activatability compared to young cells.
Cytosolic components were essential for optimal PLD activation.
A defective membrane component in senescent cells impaired PLD activation, potentially involving the PLD enzyme, PKC, or ARF.
Ceramide treatment reduced PLD activity, suggesting it mediates the inhibition.

Conclusions:

The membrane component's defect in activating PLD is a key factor in cellular senescence.
Ceramide acts as a mediator for PLD inhibition during senescence.
Understanding these mechanisms is crucial for comprehending cellular aging and regulation.