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Paper Information

Title: 

THE ROLE OF LYSOPHOSPHATIDIC ACID-INDUCED STIMULATION OF A CALCIUMDEPENDENT K+ CHANNEL ON BAVSM CELLS AND THEIR POSSIBLE INVOLVEMENT IN ATHEROSCLEROSIS PREVENTIO

Type: SPEECH
Author(s): MALIHI GOL ROKH*,ELSON E.
 
 *DEPARTMENT OF BIOCHEMISTRY AND MOLECULAR BIOPHYSICS, SCHOOL OF MEDICINE, WASHINGTON UNIVERSITY IN ST. LOUIS
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Background: Ischaemic vascular diseases are the leading cause of morbidity and mortality in developed countries, and their underlying cause is atherosclerosis. Lysophosphatidic acid (LPA), a growth factor –like biogenic lipid, has been implicated in the development of atherogenesis. High concentrations of LPA induce calcium- activated chloride current mainly via activation of Gq family of G proteins, while the threshold concentrations activate G0 proteins through a calcium dependent 2pK+ channel (TREK and TRAAK channels). We hypothesize that stimulation of this channel through LPA with threshold concentrations should prevent proliferation and calcification in bovine vascular smooth muscle cells (BAVSMCs) leading to the prevention of atherosclerosis.
Method: 5 Groups of plated BAVSMCs cultured for 48 hours in 10% CCS, replaced with SFM supplemented with LPA (10-9 -10-6 M concentrations vs control) for 4 days .The proliferation of BASMCs was assessed using hemocytometry. Calcification of the BASMCs was measured in the presence of different concentrations of LPA using β- glycerophosphate +sodium ascorbate. After 7 days, the groups of plated BASMCs were fixed and stained with Alizarin red for calcification measurement.
Results: Our preliminary experiments on bovine smooth muscle cells have shown that the effect of different concentrations of LPA can cause a dose dependent increase in proliferation of BASMCs. Only nano- molar concentrations caused a decrease in proliferation compared to control. Studies on the LPA-induced calcification have also been performed. The results have shown an increased calcification vs. LPA conc. Only nano molar concentrations have shown less mineralization compared to control. Because LPA only with nanomolar (threshold) concentrations can stimulate K2p domain channels, therefore it is suggested that LPA threshold concentrations can prevent atherosclerosis through K+ channel-induced prevention of proliferation and calcification of the BVSMCs. This study may indicate the role of the novel pathways of LPA in the prevention of atherosclerosis.

 
Keyword(s): LYSOPHOSPHATIDIC ACID, VASCULAR SMOOTH MUSCLE CELL, CELL SIGNALLING, ATHEROSCLEROSIS
 
 
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