Document Detail

Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells from Patients with Chronic Heart Failure: Role for Impaired in vivo Neovascularization and Cardiac Repair Capacity.
MedLine Citation:
PMID:  23136161     Owner:  NLM     Status:  Publisher    
BACKGROUND: MicroRNAs are key regulators of angiogenic processes. Administration of angiogenic early outgrowth cells (EOCs) or CD34(+)-cells has been suggested to improve cardiac function after ischemic injury in particular by promoting neovascularization. The present study therefore examines regulation of angiomiRs, microRNAs involved in angiogenesis, in angiogenic-EOCs and circulating CD34(+)-cells from patients with chronic heart failure (CHF) and the role for their cardiac repair capacity. METHODS AND RESULTS: Angiogenic-EOCs and CD34(+)-cells were isolated from patients with CHF due to ischemic cardiomyopathy (n=45) and healthy subjects (HS; n=35). In flow-cytometry analyses angiogenic-EOCs were largely myeloid and positive for alternatively-activated, M2-macrophage markers. In vivo cardiac neovascularization and functional repair capacity were examined after transplantation into nude mice with myocardial infarction (MI). Cardiac transplantation of angiogenic-EOCs from HS markedly increased neovascularization and improved cardiac function, whereas no such effect was observed after transplantation of angiogenic-EOCs from patients with CHF. RT-PCR analysis of 14 candidate angiomiRs, expressed in angiogenic-EOCs, revealed a pronounced loss of angiomiR-126 and -130a in angiogenic-EOCs from patients with CHF, that was also observed in circulating CD34(+)-cells. Anti-miR-126 transfection markedly impaired the capacity of angiogenic-EOCs from HS to improve cardiac function. miR-126-mimic transfection increased the capacity of angiogenic-EOCs from patients with CHF to improve cardiac neovascularization and function. CONCLUSIONS: The present study reveals a loss of angiomiR-126 and -130a in angiogenic-EOCs and circulating CD34(+)-cells from patients with CHF. Reduced miR-126 expression was identified as a novel mechanism limiting their capacity to improve cardiac neovascularization and function that can be targeted by miR-126-mimic-transfection.
Philipp Jakob; Carola Doerries; Sylvie Briand; Pavani Mocharla; Nicolle Kränkel; Christian Besler; Maja Mueller; Costantina Manes; Christian Templin; Christof Baltes; Markus Rudin; Heiner Adams; Mathias Wolfrum; Georg Noll; Frank Ruschitzka; Thomas Lüscher; Ulf Landmesser
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-11-7
Journal Detail:
Title:  Circulation     Volume:  -     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-8     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
1 University of Zurich, Zurich, Switzerland;
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