The Effect of Mineralocorticoid Receptor Antagonists on Recruitment and Function of Endothelial Progenitor Cells in Patients with Congestive Heart Failure

被引:0
作者
Levi, Amos [1 ,3 ]
Leshem-Lev, Dorit [2 ,3 ]
Weissler-Snir, Adaya [1 ,3 ]
Hasin, Tal [1 ,3 ]
Mats, Israel [1 ,3 ]
Murninkas, Daniel [1 ,3 ]
Kornowski, Ran [1 ,3 ]
Lev, Eli I. [1 ,2 ,3 ]
Ben-Gal, Tuvia [1 ,3 ]
机构
[1] Rabin Med Ctr, Dept Cardiol, Beilinson Campus, IL-4941492 Petah Tiqwa, Israel
[2] Rabin Med Ctr, Felsenstein Med Res Ctr, Petah Tiqwa, Israel
[3] Tel Aviv Univ, Sackler Fac Med, Tel Aviv, Israel
来源
ISRAEL MEDICAL ASSOCIATION JOURNAL | 2018年 / 20卷 / 04期
关键词
congestive heart failure (CHF); circulating endothelial progenitor cells (EPCs); mineralocorticoid receptor (MR) antagonists; MYOCARDIAL-INFARCTION; BONE-MARROW; ALDOSTERONE; SPIRONOLACTONE; DYSFUNCTION; EXPRESSION; NUMBER; EPLERENONE; CAPACITY; CD34(+);
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Circulating endothelial progenitor cells have an important role in the process of vascular repair. Impaired recruitment and function of endothelial progenitor cells is related to the pathophysiology of congestive heart failure. Endothelial progenitor cells have been shown to express the mineralocorticoid receptor. Objectives: To investigate the effect of mineralocorticoid receptor antagonists on endothelial progenitor cells in patients with heart failure. Methods: Twenty-four patients with compensated heart failure, who were not under mineralocorticoid receptor antagonist therapy, were recruited. Either eplerenone (n=8) or spironolactone (n=16) therapy was initiated. Circulating endothelial progenitor cell level, identified as the proportion of mononuclear cells expressing vascular endothelial growth factor receptor 2 (VEGFR-2), CD133, and CD34, was evaluated by flow cytometry at baseline and after 8 weeks. Following 7 days of culture, colonies were counted by microscopy and MTT assay was performed on randomly selected patients (n=12) to estimate viability. Results: Both median CD34+/VEGFR2+ and median CD133+/VEGFR2+ increased significantly (P = 0.04 and 0.02, respectively). However, the number of colonies and viability of the cells after therapy (as assessed by the MTT assay) was not significantly different compared with the baseline. Conclusions: These preliminary results suggest that mineralocorticoid receptor blockade may enhance endothelial progenitor cells recruitment in patients with compensated heart failure.
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页码:233 / 238
页数:6
相关论文
共 25 条
[1]   Circulating Proangiogenic Progenitor Cells Independently Predict Functional Capacity in Heart Failure Patients [J].
Alba, Ana C. ;
Lalonde, Spencer D. ;
Rao, Vivek ;
Walter, Stephen ;
Guyatt, Gordon H. ;
Ross, Heather J. .
CANADIAN JOURNAL OF CARDIOLOGY, 2013, 29 (06) :664-671
[2]   Potential role of endothelial progenitor cells in the pathophysiology of heart failure: Clinical implications and perspectives [J].
Andreou, Ioannis ;
Tousoulis, Dimitris ;
Tentolouris, Costas ;
Antoniades, Charalambos ;
Stefanadis, Christodoulos .
ATHEROSCLEROSIS, 2006, 189 (02) :247-254
[3]  
[Anonymous], 2006, AM J MED
[4]   Addition of spironolactone to angiotensin-converting enzyme inhibition in heart failure improves endothelial vasomotor dysfunction - Role of vascular superoxide anion formation and endothelial nitric oxide synthase expression [J].
Bauersachs, J ;
Heck, M ;
Fraccarollo, D ;
Hildemann, SK ;
Ertl, G ;
Wehling, M ;
Christ, M .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2002, 39 (02) :351-358
[5]   High plasma aldosterone levels on admission are associated with death in patients presenting with acute ST-elevation myocardial infarction [J].
Beygui, Farzin ;
Collet, Jean-Philippe ;
Benoliel, Jean-Jacques ;
Vignolles, Nicolas ;
Dumaine, Raphaelle ;
Barthelemy, Olivier ;
Montalescot, Gilles .
CIRCULATION, 2006, 114 (24) :2604-2610
[6]   Effects of homocysteine on number and activity of endothelial progenitor cells from peripheral blood [J].
Chen, JZ ;
Zhu, JH ;
Wang, XX ;
Zhu, JH ;
Xie, XD ;
Sun, J ;
Shang, YP ;
Guo, XG ;
Dai, HM ;
Hu, SJ .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2004, 36 (02) :233-239
[7]   Spironolactone increases nitric oxide bioactivity, improves endothelial vasodilator dysfunction, and suppresses vascular angiotensin I/angiotensin II conversion in patients with chronic heart failure [J].
Farquharson, CAJ ;
Struthers, AD .
CIRCULATION, 2000, 101 (06) :594-597
[8]   Circulating endothelial progenitor cells, vascular function, and cardiovascular risk [J].
Hill, JM ;
Zalos, G ;
Halcox, JPJ ;
Schenke, WH ;
Waclawiw, MA ;
Quyyumi, AA ;
Finkel, T .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (07) :593-600
[9]   Positive effect of eplerenone treatment on endothelial progenitor cells in patients with chronic heart failure [J].
Jung, Christian ;
Florvaag, Anna ;
Oberle, Volker ;
Fritzenwanger, Michael ;
Kretschmar, Daniel ;
Kuethe, Friedhelm ;
Betge, Stefan ;
Goebel, Bjoern ;
Franz, Marcus ;
Barz, Dagmar ;
Ferrari, Markus ;
Figulla, Hans R. .
JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM, 2012, 13 (03) :401-406
[10]   Selective functional exhaustion of hematopoietic progenitor cells in the bone marrow of patients with postinfarction heart failure [J].
Kissel, Christine K. ;
Lehmann, Ralf ;
Assmus, Birgit ;
Aicher, Alexandra ;
Honold, Joerg ;
Fischer-Rasokat, Ulrich ;
Heeschen, Christopher ;
Spyridopoulos, Ioakim ;
Dimmeler, Stefanie ;
Zeiher, Andreas M. .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2007, 49 (24) :2341-2349