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Mesoglycan attenuates VSMC proliferation through activation of AMP-activated protein kinase and mTOR

Kyung Young Lee1, Dong Hyup Lee2, Hyoung Chul Choi1

  • 1Department of Pharmacology, College of Medicine, Yeungnam University, 170 Hyunchung-Ro, Nam-Gu, Daegu, 42415 Republic of Korea ; Smart-aging Convergence Research Center, College of Medicine, Yeungnam University, 170 Hyunchung-Ro, Daegu, 42125 Republic of Korea.

Clinical Hypertension
|February 20, 2016
PubMed
Abstract

Insights

Mesoglycan activates AMP-activated protein kinase (AMPK) to inhibit vascular smooth muscle cell (VSMC) proliferation. This AMPK activation, via an mTOR-dependent pathway, offers potential therapeutic benefits for vascular proliferative disorders like atherosclerosis.

Area of Science:

  • Vascular biology
  • Cell signaling
  • Pharmacology

Background:

  • Vascular smooth muscle cell (VSMC) proliferation drives intimal thickening in atherosclerosis and restenosis.
  • Platelet-derived growth factor (PDGF) stimulates VSMC proliferation through various growth signals.
  • Mesoglycan, a glycosaminoglycan, shows vascular protective effects, but its inhibitory mechanisms on VSMC proliferation are unclear.

Purpose of the Study:

  • To investigate if mesoglycan inhibits VSMC proliferation through AMP-activated protein kinase (AMPK) activation.
  • To elucidate the underlying molecular mechanisms of mesoglycan's therapeutic effect.

Main Methods:

  • VSMCs were cultured with varying mesoglycan doses.
  • AMPK activation was assessed using western blot analysis.
  • Cell proliferation was quantified via flow cytometry.

Main Results:

  • Mesoglycan dose- and time-dependently increased AMPK phosphorylation at Thr172, and its upstream (LKB1) and downstream (ACC) targets.
  • Mesoglycan inhibited PDGF-stimulated cell cycle progression, inducing G0/G1 arrest.
  • AMPK inhibition (DNα1, DNα2, or siRNA) reversed mesoglycan's antiproliferative effect, indicating AMPK's crucial role.
  • Mesoglycan-activated AMPK signaling regulated mTOR phosphorylation, impacting cell proliferation.

Conclusions:

  • Mesoglycan-induced AMPK activation suppresses VSMC proliferation through an mTOR-dependent mechanism.
  • Mesoglycan demonstrates potential as a therapeutic agent for vascular proliferative diseases, including atherosclerosis.
Keywords:
AMPKMesoglycanProliferationVSMCmTOR

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