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Sirolimus Inhibits Platelet-Derived Growth Factor–Induced Collagen Synthesis in Rat Vascular Smooth Muscle Cells

Authors
 J. Park  ;  H. Ha  ;  H.J. Ahn  ;  S.-W. Kang  ;  Y.S. Kim  ;  J.Y. Seo  ;  M.S. Kim 
Citation
 TRANSPLANTATION PROCEEDINGS, Vol.37(8) : 3459-3462, 2005 
Journal Title
TRANSPLANTATION PROCEEDINGS
ISSN
 0041-1345 
Issue Date
2005
MeSH
Animals ; Cell Division/drug effects ; Collagen/biosynthesis* ; Collagen/drug effects ; Kinetics ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/physiology* ; Platelet-Derived Growth Factor/antagonists & inhibitors ; Platelet-Derived Growth Factor/pharmacology* ; Rats ; Reactive Oxygen Species/metabolism ; Sirolimus/pharmacology*
Keywords
16298629
Abstract
Vascular smooth muscle cell (VSMC) proliferation and extracellular matrix (ECM) accumulation play key roles in the development and the progression of vascular remodeling such as transplant arteriosclerosis and restenosis. The present study examined the effects of sirolimus (SRL) on platelet-derived growth factor (PDGF)-induced fibronectin secretion, collagen synthesis, and the related signaling pathways including reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPK) in rat VSMCs. Primary rat VSMCs were isolated from male Sprague-Dawley rats. Growth arrested, synchronized cells were treated with various concentrations of SRL before the addition of PDGF at 10 ng/mL. Proliferating cell nuclear antigen expression, fibronectin secretion, and the activation of extracellular signal-regulated protein kinase (ERK) and p38 MAPK were assessed by Western blot analysis, collagen synthesis by [(3)H]-proline incorporation, and cellular ROS by flow cytometry. PDGF (10 ng/mL) increased VSMC proliferation by 1.7-fold, fibronectin secretion by 1.5-fold, collagen synthesis by 2.1-fold, cellular ROS by 1.6-fold, and activation of ERK and p38 MAPK by 3.3- and 3.9-fold compared to controls. SRL above 1 nmol/L inhibited PDGF-induced VSMC proliferation and collagen synthesis but not PDGF-induced fibronectin secretion, cellular ROS, and activation of ERK and p38 MAPK. These data demonstrated that PDGF increased ECM synthesis as well as proliferation through cellular ROS and subsequent MAPK activation and that SRL inhibited PDGF-induced VSMC proliferation and collagen synthesis in a cellular ROS- and MAPK activation-independent way.
Full Text
http://www.sciencedirect.com/science/article/pii/S0041134505009917
DOI
10.1016/j.transproceed.2005.09.066
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Kang, Shin Wook(강신욱) ORCID logo https://orcid.org/0000-0002-5677-4756
Kim, Myoung Soo(김명수) ORCID logo https://orcid.org/0000-0002-8975-8381
Kim, Yu Seun(김유선) ORCID logo https://orcid.org/0000-0002-5105-1567
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/150571
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