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Translational and Clinical Research
Version of Record online: 18 JAN 2012
Copyright © 2011 AlphaMed Press
Volume 30, Issue 2, pages 326–335, February 2012
How to Cite
Hoke, N. N., Salloum, F. N., Kass, D. A., Das, A. and Kukreja, R. C. (2012), Preconditioning by Phosphodiesterase-5 Inhibition Improves Therapeutic Efficacy of Adipose-Derived Stem Cells Following Myocardial Infarction in Mice. STEM CELLS, 30: 326–335. doi: 10.1002/stem.789
Author contributions: N.H.: conception and design, collection and/or assembly of data, data analysis and interpretation, and manuscript writing; F.S.: conception and design, financial support, collection and/or assembly of data, data analysis and interpretation, and manuscript writing; D.K.: provision of study material; A.D.: conception and design, data analysis and interpretation, and manuscript writing; R.K.: conception and design, financial support, data analysis and interpretation, manuscript writing, and final approval of manuscript.
Disclosure of potential conflicts of interest is found at the end of this article.
First published online in STEM CELLSEXPRESS November 18, 2011.
- Issue online: 18 JAN 2012
- Version of Record online: 18 JAN 2012
- Accepted manuscript online: 18 NOV 2011 04:45PM EST
- Manuscript Accepted: 25 OCT 2011
- Manuscript Received: 8 JUL 2011
- National Institutes of Health. Grant Numbers: HL51045, HL79424, HL93685
- National Scientist Development grant from the American Heart Association. Grant Number: 10SDG3770011
- Predoctoral Fellowship from the American Heart Association. Grant Number: 09PRE2250905
Additional Supporting Information may be found in the online version of this article.
|STEM_789_sm_suppFigure1.pdf||1082K||Figure S1. Experimental Protocol. (A). In vitro protocol, arrows indicate time points for treatment, performance of simulated ischemia/reoxygenation, and measurement of various parameters for each experimental group. (B). In vivo protocol. Arrowheads indicate sites of injection of adipose-derived stem cells in the border zone of the infarcted heart.|
|STEM_789_sm_suppFigure2.pdf||957K||Figure S2. Effect of PDE-5 inhibition on protection of ASCs. Quantitative data showing the effect of sildenafil (SIL) or shRNAPDE-5 on necrosis following SI-RO as determined by MTS cell viability assay (A) and LDH release (B). (C) Representative images of TUNEL assay (10 x magnification). (* indicates p<0.01 versus SI-RO, shCON ASC; n=8).|
|STEM_789_sm_suppFigure3.pdf||955K||Figure S3. Sildenafil protects ASCs against ischemia/reoxygenation injury through PKG. Quantitative data showing the effect of KT 5823 (KT) and shRNAPKG on necrosis following SIRO as determined by MTS cell viability assay (A) and LDH release (B). (C) Representative images of TUNEL assay (10 x magnification). (* indicates p<0.01 versus SI-RO, shCON ASC; n=8).|
|STEM_789_sm_suppFigure4.pdf||1183K||Figure S4. Transplantation of preconditioned ASCs improves cardiac function and remodeling following myocardial infarction. (A) Representative M-mode images showing preservation of LV contractility of hearts treated with preconditioned ASCs as compared with non-treated ASCs control following myocardial infarction (MI). (B). Bar diagram showing quantitative data of LV fractional shortening.|
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