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Cilostazol inhibits hyperglucose-induced vascular smooth muscle cell dysfunction by modulating the RAGE/ERK/NF-κB

Sheng-Chiang Su1,2, Yi-Jen Hung3,4,5, Chia-Luen Huang1,2

  • 1Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.

Journal of Biomedical Science
|September 8, 2019
PubMed
Abstract

Insights

Cilostazol protects against high glucose-induced vascular smooth muscle cell dysfunction by inhibiting Receptor for Advanced Glycation End-products (RAGE) signaling. This study reveals novel pathways for treating diabetic vasculopathy.

Area of Science:

  • Biomedical research
  • Vascular biology
  • Diabetology

Background:

  • High glucose (HG) contributes to atherosclerosis by impairing endothelial and vascular smooth muscle cell (VSMC) function.
  • Receptor for Advanced Glycation End-products (RAGE) is implicated in diabetic macrovascular and microvascular complications.
  • Cilostazol is a therapeutic agent for diabetic vasculopathy, known to improve HG-induced vascular dysfunction.

Purpose of the Study:

  • To investigate if cilostazol's protective effects against HG-induced VSMC dysfunction involve RAGE signaling.
  • To explore the regulatory mechanisms of RAGE signaling in this context.

Main Methods:

  • Investigated the impact of HG and cilostazol on RAGE signaling in A7r5 rat VSMCs.
  • Analyzed aortic tissues from streptozotocin (STZ)-induced diabetic mice.
  • Utilized RAGE knockdown to assess its role in HG-induced VSMC dysfunction.

Main Results:

  • Diabetic mouse aortas showed reduced RAGE expression after cilostazol treatment.
  • HG upregulated RAGE, FAK, MMP-2, ICAM-1, VCAM-1, and ROS, promoting VSMC proliferation, adhesion, and migration.
  • Cilostazol reversed HG-induced changes in RAGE, ROS, gene expression, and cell functions.
  • RAGE knockdown mimicked cilostazol's effects, and combined treatment showed additive benefits on ERK/NF-κB pathways.

Conclusions:

  • Cilostazol offers protection against HG-related VSMC dysfunction through novel signal transduction pathways.
  • The study highlights the critical involvement of RAGE signaling and downstream pathways in cilostazol's therapeutic action in experimental diabetes models.
Keywords:
CilostazolDiabetesRAGEVascular smooth muscle

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