Association between microalbuminuria predicting in-stent restenosis after myocardial infarction and cellular senescence of endothelial progenitor cells

Relationship between microalbuminuria and worse outcome of coronary artery disease patients is discussed, but its underlying pathophysiological mechanism remains unclear. We investigated the role of microalbuminuria to the function of endothelial progenitor cells (EPCs), that might affect to outcome...

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Bibliographic Details
Published in:PloS one 2015-04, Vol.10 (4), p.e0123733-e0123733
Main Authors: Ota, Hisanobu, Takehara, Naofumi, Aonuma, Tatsuya, Kabara, Maki, Matsuki, Motoki, Yamauchi, Atsushi, Takeuchi, Toshiharu, Kawabe, Jun-ichi, Hasebe, Naoyuki
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Albuminuria - complications
Albuminuria - diagnosis
Angiography
Antigens, CD34 - metabolism
Atherosclerosis
Balloon angioplasty
Bone marrow
Cardiology
Cardiovascular disease
CD34 antigen
Cells (biology)
Cellular Senescence
Coronary artery
Coronary artery disease
Coronary Restenosis - complications
Coronary Restenosis - diagnosis
Coronary vessels
Diabetes
DNA damage
Endothelial Progenitor Cells - cytology
Endothelium
Excretion
Female
Fibronectin
Fibronectins
Fibronectins - metabolism
Flow Cytometry
Gene expression
Gene Expression Profiling
Glomerular Filtration Rate
Heart attack
Heart attacks
Heart diseases
Humans
Hypertension
Implants
Internal medicine
Ischemia
Lectins
Lectins - metabolism
Male
Medical imaging
Medicine
Metabolic syndrome
Middle Aged
Mortality
Myocardial infarction
Myocardial Infarction - complications
Myocardial Infarction - surgery
Nephrology
Neurology
Patients
Restenosis
Risk Factors
RNA
Senescence
Sirtuin 1 - metabolism
Stem cells
Stents
Surgical implants
Treatment Outcome
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Summary:Relationship between microalbuminuria and worse outcome of coronary artery disease patients is discussed, but its underlying pathophysiological mechanism remains unclear. We investigated the role of microalbuminuria to the function of endothelial progenitor cells (EPCs), that might affect to outcome of acute myocardial infarction (AMI) patients. Forty-five AMI patients were divided into two groups according to their urinary albumin excretion: normal (n = 24) and microalbuminuria (>30 mg/day, n = 21). At day-2 and day-7 after AMI onset, circulating-EPCs (CD34+ Flk1+) were quantified by flow cytometry. The number of lectin-acLDL-positive cultured-EPCs immobilized on fibronectin was determined. To assess the cellular senescence of cultured-EPCs, the expression level of sirtuin-1 mRNA and the number of SA-β-gal positive cell were evaluated. Angiographic late in-stent loss after percutaneous coronary intervention (PCI) was evaluated at a six-month follow-up. No significant differences in coronary risk and the extent of myocardial damage were observed between the two groups. Late in-stent loss at the six-month follow-up was significantly higher in the microalbuminuria group (normal:microalbuminuria = 0.76±0.34:1.18±0.57 mm, p=0.021). The number of circulating-EPCs was significantly increased in microalbuminuria group at day-7, however, improved adhesion of EPCs was observed in normal group but not in microalbuminuria group from baseline to day-7 (+3.1±8.3:-1.3±4.4%: p
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0123733