| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on November 16, 2003
Accepted on January 5, 2004
From the Departments of Geriatric Medicine (Y.X., X.Z.), Pediatrics (M.Y., T.H., T.N.), and Cardiovascular Medicine (T.K.), Kyoto University Graduate School of Medicine, Japan; the Translational Research Center (T.M.), Kyoto University Hospital, Kyoto, Japan; and the RIKEN Center for Developmental Biology (S.N.), Kobe, Japan
* To whom correspondence should be addressed. E-mail: harai{at}kuhp.kyoto-u.ac.jp.
Objectives--Arterial injury results in vascular remodeling associated with proliferation and migration of smooth muscle cells (SMCs) and the development of intimal hyperplasia, which is a critical component of restenosis after angioplasty of human coronary arteries and an important feature of atherosclerotic lesions. However, the origin of SMCs and other cells in the development of vascular remodeling is not yet fully understood.
Methods and Results--We utilized a cuff-induced vascular injury model after transplantation of the bone marrow (BM) from green fluorescent protein (GFP)-transgenic mice. We found that macrophages were major cells recruited to the adventitia of the vascular injury lesion along with SMCs and endothelial cells (ECs). While investigating whether those cells are derived from the donor, we found that most of the macrophages were GFP-positive, and some of the SMCs and ECs were also GFP-positive. Administration of the anti-c-fms antibody resulted in a marked decrease in macrophages and a relative increase of SMCs, while administration of antibodies against the platelet-derived growth factor receptor-
caused a prominent decrease in SMCs and a relative increase in macrophages.
Conclusions--The current study indicates that BM-derived cells play an important role in vascular injury, and that differentiation of macrophages and SMCs might be dependent on each other.
This article has been cited by other articles:
![]() |
Y. Shiba, M. Takahashi, T. Yoshioka, N. Yajima, H. Morimoto, A. Izawa, H. Ise, K. Hatake, K. Motoyoshi, and U. Ikeda M-CSF Accelerates Neointimal Formation in the Early Phase After Vascular Injury in Mice: The Critical Role of the SDF-1-CXCR4 System Arterioscler Thromb Vasc Biol, February 1, 2007; 27(2): 283 - 289. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q. Xiao, L. Zeng, Z. Zhang, A. Margariti, Z. A Ali, K. M. Channon, Q. Xu, and Y. Hu Sca-1+ Progenitors Derived From Embryonic Stem Cells Differentiate Into Endothelial Cells Capable of Vascular Repair After Arterial Injury Arterioscler Thromb Vasc Biol, October 1, 2006; 26(10): 2244 - 2251. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Schafer, M. R. Schroeter, C. Dellas, M. Puls, M. Nitsche, E. Weiss, G. Hasenfuss, and S. V. Konstantinides Plasminogen Activator Inhibitor-1 From Bone Marrow-Derived Cells Suppresses Neointimal Formation After Vascular Injury in Mice Arterioscler Thromb Vasc Biol, June 1, 2006; 26(6): 1254 - 1259. [Abstract] [Full Text] [PDF] |
||||
![]() |
L.-N. Zhang, D. W. Wilson, V. da Cunha, M. E. Sullivan, R. Vergona, J. C. Rutledge, and Y.-X. Wang Endothelial NO Synthase Deficiency Promotes Smooth Muscle Progenitor Cells in Association With Upregulation of Stromal Cell-Derived Factor-1{alpha} in a Mouse Model of Carotid Artery Ligation Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 765 - 772. [Abstract] [Full Text] [PDF] |
||||
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2004 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |