Document Detail


Cardiac progenitor cells and biotinylated insulin-like growth factor-1 nanofibers improve endogenous and exogenous myocardial regeneration after infarction.
MedLine Citation:
PMID:  19704095     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Cardiac progenitor cells (CPCs) possess the insulin-like growth factor-1 (IGF-1)-IGF-1 receptor system, and IGF-1 can be tethered to self-assembling peptide nanofibers (NF-IGF-1), leading to prolonged release of this growth factor to the myocardium. Therefore, we tested whether local injection of clonogenic CPCs and NF-IGF-1 potentiates the activation and differentiation of delivered and resident CPCs enhancing cardiac repair after infarction.
METHODS AND RESULTS: Myocardial infarction was induced in rats, and untreated infarcts and infarcts treated with CPCs or NF-IGF-1 only and CPCs and NF-IGF-1 together were analyzed. With respect to infarcts exposed to CPCs or NF-IGF-1 alone, combination therapy resulted in a greater increase in the ratio of left ventricular mass to chamber volume and a better preservation of +dP/dt, -dP/dt, ejection fraction, and diastolic wall stress. Myocardial regeneration was detected in all treated infarcts, but the number of newly formed myocytes with combination therapy was 32% and 230% higher than with CPCs and NF-IGF-1, respectively. Corresponding differences in the volume of regenerated myocytes were 48% and 115%. Similarly, the length density of newly formed coronary arterioles with both CPCs and NF-IGF-1 was 73% and 83% greater than with CPCs and NF-IGF-1 alone, respectively. Importantly, activation of resident CPCs by paracrine effects contributed to cardiomyogenesis and vasculogenesis. Collectively, CPCs and NF-IGF-1 therapy reduced infarct size more than CPCs and NF-IGF-1 alone.
CONCLUSIONS: The addition of nanofiber-mediated IGF-1 delivery to CPC therapy improved in part the recovery of myocardial structure and function after infarction.
Authors:
M Elena Padin-Iruegas; Yu Misao; Michael E Davis; Vincent F M Segers; Grazia Esposito; Tomotake Tokunou; Konrad Urbanek; Toru Hosoda; Marcello Rota; Piero Anversa; Annarosa Leri; Richard T Lee; Jan Kajstura
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-08-24
Journal Detail:
Title:  Circulation     Volume:  120     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-09     Completed Date:  2009-10-07     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  876-87     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesia and Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological
Animals
Apoptosis
Biotin*
Cell Fusion
Cell Proliferation
Cells, Cultured
Coronary Vessels / physiopathology
Female
Insulin-Like Growth Factor I / administration & dosage*
Myocardial Infarction / pathology,  physiopathology*,  surgery*
Myocardium / pathology
Myocytes, Cardiac* / pathology
Nanostructures*
Rats
Rats, Inbred F344
Regeneration* / drug effects
Stem Cell Transplantation*
Stem Cells*
Tissue Survival
Ventricular Function
Grant Support
ID/Acronym/Agency:
EB003805/EB/NIBIB NIH HHS; R01 HL065573-07/HL/NHLBI NIH HHS; R01 HL075480-05/HL/NHLBI NIH HHS; R21 HL094894-01/HL/NHLBI NIH HHS; R21 HL094894-01S1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
58-85-5/Biotin; 67763-96-6/Insulin-Like Growth Factor I
Comments/Corrections
Comment In:
Circulation. 2009 Sep 8;120(10):831-4   [PMID:  19704092 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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