JTCS Sign the Guestbook
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Joel Price
Thierry G. Mesana
Marc Ruel
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Suuronen, E. J.
Right arrow Articles by Ruel, M.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Suuronen, E. J.
Right arrow Articles by Ruel, M.
Related Collections
Right arrow Myocardial infarction

J Thorac Cardiovasc Surg 2007;134:1249-1258
© 2007 The American Association for Thoracic Surgery

Evolving Technology

Comparative effects of mesenchymal progenitor cells, endothelial progenitor cells, or their combination on myocardial infarct regeneration and cardiac function

Erik J. Suuronen, PhDa,b, Joel Price, MDa, John P. Veinot, MDc, Kathryn Ascah, MDd, Varun Kapila, MDa, Xue-Wei Guo, MD, PhDa, Serena Wong, MSca,b, Thierry G. Mesana, MD, PhDa, Marc Ruel, MD, MPHa,b,*

a Division of Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
d Division of Cardiology, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
b Department of Cellular and Molecular Medicine, University of Ottawa Heart Institute, Ottawa, Ontario, Canada
c Department of Pathology and Laboratory Medicine, University of Ottawa Heart Institute, Ottawa, Ontario, Canada.

Received for publication March 6, 2007; revisions received June 29, 2007; accepted for publication July 16, 2007.

* Address for reprints: Marc Ruel, MD, MPH, University of Ottawa Heart Institute, Division of Cardiac Surgery, 40 Ruskin St, Laboratory H553, Ottawa, Ontario, Canada, K1Y 4W7. (Email: mruel{at}ottawaheart.ca).

Objective: Recent evidence suggests that the effects of mesenchymal progenitor cell transplantation into the infarcted myocardium might be mediated by local paracrine angiogenesis. We compared the effects of mesenchymal progenitor cell transplantation versus those of a primarily angiogenic cell, the endothelial progenitor cell, in a rat model of myocardial infarction.

Methods: Twenty-one days after left anterior descending artery ligation, rats were injected in their infarcted anterior myocardium with 1 x 106 mesenchymal progenitor cells, 1 x 106 endothelial progenitor cells, 5 x 105 mesenchymal progenitor cells plus 5 x 105 endothelial progenitor cells, or phosphate-buffered saline (n = 6-8 per group). Echocardiography was performed before injection and 4 weeks later, after which rats were killed and immunohistochemical analyses performed.

Results: Connexin43 density was greater in cell-treated groups compared with that seen in the phosphate-buffered saline group (by 91.6% ± 15.2%, P < .001), with no observed difference between cell-treated groups (P ≥ .3). Endothelial progenitor cell treatment increased arteriolar density within the infarct border zone (by 297%, 205%, and 101% vs phosphate-buffered saline, mesenchymal progenitor cell, and mesenchymal progenitor cell/endothelial progenitor cell treatment, respectively; P < .01). Postoperative left ventricular ejection fraction (endothelial progenitor cell: 68.3% ± 9.8% vs mesenchymal progenitor cell/endothelial progenitor cell: 55.0% ± 11.1%, mesenchymal progenitor cell: 53.0% ± 6.0%, and phosphate-buffered saline: 49.6% ± 9.5%) and fractional shortening (endothelial progenitor cell: 32.4% ± 5.1% vs mesenchymal progenitor cell: 22.5% ± 5.4% and phosphate-buffered saline: 21.3% ± 5.3%) were greater in endothelial progenitor cell–treated rats versus those receiving other treatments (all P < .05). Only endothelial progenitor cells prevented further contractile deterioration compared with baseline values (P = .8), whereas other groups had continued loss of function after treatment.

Conclusion: Compared with the use of mesenchymal progenitor cells, cell transplantation with endothelial progenitor cells after myocardial infarction resulted in better neovascularization and contractility. This suggests that angiogenesis is an important mechanism in attenuating the progression of left ventricular dysfunction after myocardial infarction.

Abbreviations and Acronyms EPC = endothelial progenitor cell; FS = fractional shortening; HPS = hematoxylin-phloxine-saffron; LV = left ventricular; LVEF = left ventricular ejection fraction; LVID = left ventricular internal dimension; MI = myocardial infarction; MPC = mesenchymal progenitor cell; PBS = phosphate-buffered saline




This article has been cited by other articles:


Home page
 Circ. Res.Home page
M. Ruel, A. F.R. Stewart, and E. J. Suuronen
From Genes to Regenerative Medicine: Approaches in Development
Circ. Res., November 7, 2008; 103(10): 1050 - 1052.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 2007 by The American Association for Thoracic Surgery.