Physiol. Genomics Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Physiol. Genomics 30: 44-52, 2007. First published February 27, 2007; doi:10.1152/physiolgenomics.00070.2006
1094-8341/07 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figures and Tables
Right arrow All Versions of this Article:
30/1/44    most recent
00070.2006v1
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 Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Haris Naseem, R.
Right arrow Articles by Garry, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haris Naseem, R.
Right arrow Articles by Garry, D. J.
Received 24 April 2006; accepted in final form 23 February 2007.
Physiological Genomics 30:44-52 (2007)
1094-8341/07 $8.00 © 2007 American Physiological Society

Reparative myocardial mechanisms in adult C57BL/6 and MRL mice following injury

R. Haris Naseem1, Annette P. Meeson1, J. Michael DiMaio2, Michael D. White2, Justin Kallhoff1, Caroline Humphries1, Sean C. Goetsch1, Leon J. De Windt3, Maurice A. Williams1, Mary G. Garry1 and Daniel J. Garry1,4,5

1 Departments of Internal Medicine and
2 Cardiothoracic Surgery, University of Texas Southwestern Medical Center, Dallas, Texas
3 Hubrecht Laboratory and Interuniversity Cardiology Institute Netherlands, Royal Netherlands Academy of Arts and Sciences, Utrecht, The Netherlands
4 Department of Molecular Biology, University of Texas Southwestern Medical Center, and
5 Donald W. Reynolds Cardiovascular Clinical Research Center at UT Southwestern Medical Center, Dallas, Texas

Previous studies have suggested that the heart may be capable of limited repair and regeneration in response to a focal injury, while other studies indicate that the mammalian heart has no regenerative capacity. To further explore this issue, we performed a series of superficial and transmural myocardial injuries in C57BL/6 and MRL/MpJ adult mice. At defined time intervals following the respective injury (days 3, 14, 30 and 60), we examined cardiac function using echocardiography, morphology, fluorescence-activated cell sorting for 5-bromo-2-deoxyuridine-positive cells and molecular signature using microarray analysis. We observed restoration of myocardial function in the superficial MRL cryoinjured heart and significantly less collagen deposition compared with the injured hearts of C57BL/6 mice. Following a severe transmural myocardial injury, the MRL mouse has increased survival and decreased ventricular remodeling compared with the C57BL/6 mouse but without evidence of complete regeneration. The cytoprotective program observed in the severely injured MRL heart is in part due to increased cellular proliferation, increased vasculogenesis, and decreased apoptosis that limits the extension of the injury. We conclude that MRL injured hearts have evidence of myocardial regeneration, in response to superficial injury, but the stabilized left ventricular function and improved survival observed in the MRL mouse following severe injury is not associated with complete myocardial regeneration.

myocardial regeneration; cytoprotection; progenitor cells; echocardiography; TUNEL assay; transcriptome analysis






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2007 by the American Physiological Society.