Association between microalbuminuria predicting in-stent restenosis after myocardial infarction and cellular senescence of endothelial progenitor cells.
Association between microalbuminuria predicting in-stent restenosis after myocardial infarction and cellular senescence of endothelial progenitor cells.
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微量白蛋白尿症预测心肌梗塞后的内部再狭窄和内皮祖细胞的细胞衰老。
DOI：
10.1371/journal.pone.0123733
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Hasebe N
中科院分区：
文献类型：
--
作者：
Ota H;Takehara N;Aonuma T;Kabara M;Matsuki M;Yamauchi A;Takeuchi T;Kawabe J;Hasebe N
微量白蛋白尿与冠心病患者预后不良的关系已被讨论，但其潜在的病理生理机制尚不清楚。本研究探讨了微量白蛋白尿对内皮祖细胞功能的影响，从而可能影响急性心肌梗死（AMI）患者的预后。45例AMI患者根据尿白蛋白排泄量分为两组：正常组（n = 24）和微量白蛋白尿（>30 mg/天，n = 21）。在AMI发病后第2天和第7天，通过流式细胞术定量循环EPCs（CD 34 + Flk 1+）。测定固定在纤连蛋白上的凝集素-acLDL阳性培养的EPCs的数量。通过检测Sirtuin-1 mRNA表达水平和SA-β-gal阳性细胞数来评价体外培养的EPCs的衰老情况。在六个月随访时评估了经皮冠状动脉介入治疗（PCI）后血管造影晚期支架内丢失。两组间冠状动脉风险和心肌损伤程度无显著差异。6个月随访时，微量白蛋白尿组的晚期支架内丢失显著较高（正常：微量白蛋白尿= 0.76±0.34：1.18±0.57 mm，p=0.021）。第7天微量白蛋白尿组循环内皮祖细胞数量显著增加，而正常组内皮祖细胞粘附能力改善，但微量白蛋白尿组从基线至第7天未观察到（+3.1 8. 3：-1.3 4. 4%：p<0.05）。而微量白蛋白尿组第7天培养的EPCs的sirtuin-1 mRNA表达水平显著降低（7.1±8.9：2.5±3.7倍，p<0.05），这是基于sirtuin-1 mRNA表达水平与微量白蛋白尿程度呈负相关。微量白蛋白尿组SA-β-gal阳性细胞比例较正常组明显增加。AMI患者微量白蛋白尿通过细胞衰老与内皮祖细胞功能紊乱密切相关，预示PCI术后冠状动脉重构加重。
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<0.05). On the other hand, in microalbuminuria group at day-7, the level of sirtuin-1 mRNA expression of cultured-EPCs was significantly decreased (7.1±8.9 : 2.5±3.7 fold, p<0.05), which was based on the negative correlation between the level of sirtuin-1 mRNA expression and the extent of microalbuminuria. The ratio of SA-β-gal-positive cells in microalbuminuria group was increased compared to that of normal group. Microalbuminuria in AMI patients is closely associated with functional disorder of EPCs via cellular senescence, that predicts the aggravation of coronary remodeling after PCI.
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