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Related Experiment Video

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ox-LDL induces endothelial dysfunction by promoting Arp2/3 complex expression.

Yao Tang1, Jianting Zhao1, Liming Shen1

  • 1Vascular Surgery, Suzhou Municipal Hospital, Suzhou Hospital Affiliated to Nanjing Medical University, 26 Daoqian Street, Suzhou, Jiangsu 215002, PR China.

Biochemical and Biophysical Research Communications
|May 17, 2016
PubMed
Summary

Oxidized low-density lipoproteins (ox-LDL) trigger endothelial dysfunction by upregulating the actin-related protein 2/3 (Arp2/3) complex via LOX-1/Rac-1 signaling. Inhibiting Arp2/3 complex reduces damage and improves endothelial function.

Keywords:
Arp2/3Endothelial dysfunctionLOX-1Rac-1ox-LDL

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Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Oxidized low-density lipoproteins (ox-LDL) are key contributors to endothelial injury and dysfunction.
  • Cytoskeleton reorganization, particularly involving the actin-related protein 2/3 (Arp2/3) complex, is implicated in ox-LDL-induced endothelial damage.

Purpose of the Study:

  • To elucidate the role of the Arp2/3 complex in ox-LDL-induced endothelial dysfunction.
  • To investigate the signaling pathways involved in Arp2/3 complex regulation by ox-LDL.

Main Methods:

  • Assessed Arp2 and Arp3 expression in ApoE-/- mice and ox-LDL-stimulated human coronary artery endothelial cells (HCAECs).
  • Utilized the Arp2/3 complex inhibitor CK666 to evaluate its effects on ox-LDL-induced cellular responses.
  • Investigated the involvement of LOX-1 and CD36 receptors using blocking antibodies.
  • Employed Rac-1 siRNA to determine its impact on Arp2/3 expression.

Main Results:

  • Arp2 and Arp3 expression increased under atherosclerotic conditions and upon ox-LDL stimulation.
  • CK666 treatment attenuated ox-LDL-induced reactive oxygen species (ROS) generation and cytoskeleton reorganization, while enhancing nitric oxide (NO) release in HCAECs.
  • LOX-1 blockade, but not CD36 blockade, reduced ox-LDL-induced Arp2 and Arp3 expression.
  • Rac-1 siRNA significantly suppressed ox-LDL-stimulated Arp2 and Arp3 expression.
  • CK666 administration decreased endothelial nitric oxide synthase (eNOS) expression and atherosclerotic lesion size in ApoE-/- mice.

Conclusions:

  • Oxidized low-density lipoproteins induce endothelial dysfunction through the activation of the LOX-1/Rac-1 signaling pathway.
  • This activation leads to the upregulation of the Arp2/3 complex, contributing to cellular damage.
  • Targeting the Arp2/3 complex may offer a therapeutic strategy for atherosclerosis and related endothelial dysfunction.