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Rac3, but not Rac1, promotes ox-LDL induced endothelial dysfunction by downregulating autophagy.

Dan He1,2,3, Ling Xu4, Yuhang Wu1

  • 1Institute of Heart and Vessel Diseases, The Second Affiliated Hospital of Dalian Medical University, Dalian Medical University, Dalian, China.

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Summary
This summary is machine-generated.

Reduced levels of Rac1 and Rac3 proteins protect against oxidized LDL-induced endothelial dysfunction by inhibiting autophagy, with Rac3 showing a more significant protective effect.

Keywords:
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Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanisms of Atherosclerosis
  • Molecular Signaling in Endothelial Cells

Background:

  • Endothelial dysfunction, driven by oxidized low-density lipoprotein (ox-LDL), is a key factor in atherosclerosis development, involving oxidative stress and inflammation.
  • The role of autophagy, a cellular self-degradation process, in atherosclerosis is gaining significant research interest.
  • Ras-related C3 botulinum toxin substrate 1 (Rac1) and Rac3 are small GTPases implicated in cellular processes, but their specific role in ox-LDL-induced endothelial dysfunction and autophagy remains unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms by which Rac1 and Rac3 influence endothelial cell inflammation and dysfunction induced by ox-LDL.
  • To determine if the anti-inflammatory effects of Rac1 and Rac3 in endothelial cells are mediated through the regulation of autophagy.
  • To compare the relative contributions of Rac1 and Rac3 in these processes, both in vitro and in vivo.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) with knockdown of Rac1 and Rac3 were treated with ox-LDL.
  • Inflammatory factors, autophagy proteins, reactive oxygen species (ROS), and foam cell formation were assessed.
  • The autophagy inhibitor 3-methyladenine (3-MA) was used to explore the role of autophagy in Rac1/Rac3-mediated effects. ApoE-/- mice were used for in vivo validation.

Main Results:

  • Knockdown of Rac1 and Rac3 in HUVECs attenuated ox-LDL-induced endothelial dysfunction, including reduced inflammatory markers like NF-κB and NLRP3, and decreased ROS production.
  • Inhibition of autophagy using 3-MA in Rac1 and Rac3 knockdown cells reversed the protective effects, indicating that Rac1/Rac3 exert their benefits by modulating autophagy.
  • Rac3 demonstrated a more pronounced protective effect compared to Rac1 in mitigating ox-LDL-induced endothelial injury.

Conclusions:

  • Rac1 and Rac3 play a critical role in ox-LDL-induced endothelial dysfunction, primarily through the regulation of autophagy.
  • The anti-inflammatory and protective effects of Rac1 and Rac3 against ox-LDL involve the inhibition of autophagy.
  • Rac3 is a more significant regulator than Rac1 in this context, suggesting potential therapeutic targeting for atherosclerosis.