Loss of AngiomiR-126 and 130a in Angiogenic Early Outgrowth Cells From Patients With Chronic Heart Failure
Key result
Patients with chronic heart failure exhibited a pronounced loss of angiomiR-126 and -130a in angiogenic EOCs and circulating CD34(+) cells, which limited their cardiac repair capacity.
Why the study?
Does miR-126 mimic transfection improve the cardiac neovascularization and functional repair capacity of angiogenic EOCs from patients with chronic heart failure?
Population
Angiogenic early outgrowth cells and CD34 cells isolated from patients with chronic heart failure caused by…
Comparison
Transplantation of angiogenic EOCs transfected… vs Transplantation of unmodified EOCs from healthy…
Design
Preclinical
Authors
Discussion
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Implication
Reduced angiomiR-126/130a in CHF-derived EOCs and CD34+ cells may impair repair; hypothesis-generating for miRNA modulation before clinical translation.
Study Design
Type
Observational (n=80)
Structured PICO
Does miR-126 mimic transfection improve the cardiac neovascularization and functional repair capacity of angiogenic EOCs from patients with chronic heart failure?
P
Population
80 subjects, including 45 patients with chronic heart failure caused by ischemic cardiomyopathy and 35 healthy subjects.
E
Exposure
Transplantation of angiogenic EOCs transfected with miR-126 mimic or anti-miR-126
C
Comparator
Transplantation of unmodified EOCs from healthy subjects or CHF patients
O
Outcome
Cardiac neovascularization and functional repair capacity in vivo, and angiomiR expression levelssurrogate
Reduced miR-126 expression in angiogenic EOCs from CHF patients limits their cardiac repair capacity, which can be restored by miR-126 mimic transfection.
Cite This Study
Jakob et al. (2012) conducted an observational in Chronic heart failure (n=80). Chronic heart failure vs. Healthy subjects was evaluated on Expression of angiomiR-126 and -130a in angiogenic EOCs and circulating CD34(+) cells. Patients with chronic heart failure exhibited a pronounced loss of angiomiR-126 and -130a in angiogenic EOCs and circulating CD34(+) cells, which limited their cardiac repair capacity.