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Rac1 modification by an electrophilic 15-deoxy Δ(12,14)-prostaglandin J2 analog.

S B Wall1, J-Y Oh1, L Mitchell2

  • 1Center for Free Radical Biology and Department of Pathology, University of Alabama at Birmingham, AL, USA.

Redox Biology
|February 14, 2015
PubMed
Summary

15-deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2) modifies the GTPase Rac1 in vascular endothelial cells (ECs). This electrophilic lipid adduct formation alters Rac1 activity, impacting EC function and potentially contributing to cardiovascular diseases.

Keywords:
CyclopentenoneElectrophile responsive proteomeOxidative post-translational modificationRedox signalingRho GTPaseThiol

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Area of Science:

  • Vascular biology
  • Redox signaling
  • Molecular cell biology

Background:

  • Vascular endothelial cells (ECs) maintain vascular homeostasis, and their dysfunction is implicated in cardiovascular diseases.
  • The GTPase Rac1 is crucial for EC responses to stress, regulating cytoskeletal dynamics and cell junctions.
  • Rac1 activity is modulated by redox modifications like glutathiolation and S-nitrosation.

Purpose of the Study:

  • To investigate whether the redox signaling mediator 15-deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2) modulates Rac1 activity in ECs.
  • To identify specific modification sites on Rac1 by 15d-PGJ2.
  • To determine the functional consequences of Rac1 modification by 15d-PGJ2 on EC behavior.

Main Methods:

  • In vitro adduction assays using a biotin-tagged analog of 15d-PGJ2 (bt-15d-PGJ2).
  • Mass spectrometry to identify Rac1 modification sites (C157 and C178).
  • Experiments in cultured ECs to assess Rac1 activity, modification, migration, and cell spreading.

Main Results:

  • Bt-15d-PGJ2 formed adducts with Rac1 at C157 and C178 in vitro.
  • Rac1 modification and altered activity by bt-15d-PGJ2 were observed in cultured ECs.
  • 15d-PGJ2 treatment led to decreased EC migration and cell spreading.

Conclusions:

  • Rac1 is a direct molecular target of 15d-PGJ2 in vascular endothelial cells.
  • Modification of Rac1 by electrophiles like 15d-PGJ2 can alter its activity and EC function.
  • These findings suggest a novel mechanism by which redox signaling impacts vascular health and disease.