Effects of glucocorticoids and mineralocorticoids on proliferation and maturation of human peripheral blood stem cells

Grafte-Faure, Stéphanie; Leveque, Catherine; Vasse, Marc; Soria, Claudine; Norris, Victor; Vannier, Jean‐Pierre

doi:10.1002/(sici)1096-8652(199910)62:2<65::aid-ajh1>3.0.co;2-g

Cited by 18 publications

(12 citation statements)

References 39 publications

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“…Our finding that CD34+ cells express the mineralocorticoid receptor is consistent with accumulating evidence that circulating progenitor cells express mineralocorticoid receptors 28, 29 and also that their growth in vitro is impaired by addition of aldosterone to the culture medium. 14 These findings are made all the more compelling by the observed reversal of these effects in vitro with the addition of spironolactone.…”

Section: Discussionsupporting

confidence: 91%

Regulation of Circulating Progenitor Cells in Left Ventricular Dysfunction

Boilson

Larsen

Harbuzariu

et al. 2010

Circ: Heart Failure

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Background Reductions in numbers of circulating progenitor cells (CD34+ cell subsets) have been demonstrated in patients at risk for, or in the presence of, cardiovascular disease. The mediators of these reductions remain undefined. To determine whether neurohumoral factors might regulate circulating CD34+ cell subsets in vivo, we studied complementary canine models of left ventricular (LV) dysfunction. Methods and Results A pacing model of severe LV dysfunction and a hypertensive renal wrap (RW) model in which dogs were randomized to receive deoxycorticosterone acetate (DOCA) were studied. Circulating CD34+ cell subsets including hematopoietic precursor cells (HPCs:CD34+/CD45dim/VEGFR2-) and endothelial progenitor cells (EPCs:CD34+/CD45-/VEGFR2+) were quantified. Additionally, the effect of mineralocorticoid excess on circulating progenitor cells in normal dogs was studied. The majority of circulating CD34+ cells expressed CD45 dimly and did not express VEGFR2, consistent with an HPC phenotype. HPCs were decreased in response to pacing, and this decrease correlated with plasma aldosterone levels (Spearman Rank correlation = -0.67, p=0.03). In the RW model, administration of DOCA resulted in decreased HPCs. No changes were seen in EPCs in either model. Normal dogs treated with DOCA exhibited a decrease in HPCs in peripheral blood but not bone marrow associated with decreased telomerase activity. Conclusions This is the first study to demonstrate that mineralocorticoid excess, either endogenous or exogenous, results in reduction in HPCs. These data suggest that mineralocorticoids may induce accelerated senescence of progenitor cells leading to their reduced survival and decline in numbers.

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Section: Discussionsupporting

confidence: 91%

Regulation of Circulating Progenitor Cells in Left Ventricular Dysfunction

Boilson

Larsen

Harbuzariu

et al. 2010

Circ: Heart Failure

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“…Moreover, steroids are well known to influence the development, differentiation and homeostasis of a large number of cells. In particular, glucocorticoids (GC) affect the differentiation of several types of stem cells such as mesenchymal [24] and neural stem [25] cells in vitro, and also have an effect on the proliferation and maturation of human peripheral blood stem cells in vitro and in vivo [26]. The migratory capacity and relative baseline levels of CD133+ cells may be influenced by chronic steroid therapy.…”

Section: Discussionmentioning

confidence: 99%

Correlation of Circulating CD133+ Progenitor Subclasses with a Mild Phenotype in Duchenne Muscular Dystrophy Patients

et al. 2008

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BackgroundVarious prognostic serum and cellular markers have been identified for many diseases, such as cardiovascular diseases and tumor pathologies. Here we assessed whether the levels of certain stem cells may predict the progression of Duchenne muscular dystrophy (DMD).Methods and FindingsThe levels of several subpopulations of circulating stem cells expressing the CD133 antigen were determined by flow cytometry in 70 DMD patients. The correlation between the levels and clinical status was assessed by statistical analysis. The median (±SD) age of the population was 10.66±3.81 (range 3 to 20 years). The levels of CD133+CXCR4+CD34- stem cells were significantly higher in DMD patients compared to healthy controls (mean±standard deviation: 17.38±1.38 vs. 11.0±1.70; P = 0.03) with a tendency towards decreased levels in older patients. Moreover, the levels of this subpopulation of cells correlated with the clinical condition. In a subgroup of 19 DMD patients after 24 months of follow-up, increased levels of CD133+CXCR4+CD34- cells was shown to be associated with a phenotype characterised by slower disease progression. The circulating CD133+CXCR4+CD34- cells in patients from different ages did not exhibit significant differences in their myogenic and endothelial in vitro differentiation capacity.ConclusionsOur results suggest that levels of CD133+CXCR4+CD34- could function as a new prognostic clinical marker for the progression of DMD.

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“…It has been reported that aldosterone increases the colony formation/proliferation of granulocyte-macrophage cells and diminishes the same parameters for erythroid cells. 14 Recent experiments have shown a downregulation of the mRNAs for proliferative proto-oncogenes by aldosterone. 15 In contrast, aldosterone may mediate angiotensin II-stimulated vascular smooth muscle cell proliferation in vitro.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone and d -Glucose Stimulate the Proliferation of Human Cardiac Myofibroblasts In Vitro

et al. 2002

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Abstract-The renin-angiotensin-aldosterone-system appears to be involved in the development of cardiac fibrosis in rodents, characterized by nonepithelial cell proliferation and changes in the extracellular matrix. The aim of our study was to investigate the effect of high aldosterone concentrations on the proliferation of human cardiac interstitial cells in vitro. In addition, the effect of D-glucose as another risk factor for fibrosis, eg, in the diabetic heart, was investigated. Human cardiac myofibroblast cultures were established, and growth rates were measured by WST-1 assay in fetal calf serum-free Dulbecco's modified Eagle's medium (DMEM). Cells in culture showed a significant increase in number between 24 to 72 hours of cultivation under basal conditions (DMEM, 10% fetal calf serum). Aldosterone at high concentrations (10 Ϫ8 and 10 Ϫ7 mol/L) significantly (PϽ0.01) increased the proliferation of cultured cardiac myofibroblasts. Comparable effects were observed after incubation of the cells with high D-glucose concentrations (15 and 25 mmol/L, PϽ0.01). No additive growth stimulation was evident when the cells were incubated in medium containing both aldosterone and D -glucose. These results suggest a role for aldosterone and glucose in mediating the cardiac fibrosis through stimulation of myofibroblast growth in patients with dysregulated renin-angiotensin-aldosterone-system (especially hyperaldosteronism) and impaired glucose homeostasis. R ecent clinical studies demonstrate a reduction in cardiovascular mortality in patients with heart failure treated with ACE inhibitors, angiotensin II blockers, and aldosterone antagonists. These effects were also seen in patients with diabetes mellitus. Ramipril reduced not only cardiac failure and myocardial infarction but also diabetic complications and the incidence of new manifestations of diabetic disease. 1 In the RALES trial (Randomized Aldactone Evaluation Study), spironolactone added to standard therapy (ACE inhibitors, loop diuretics, digoxin, etc) had a beneficial effect on mortality in patients with congestive heart failure, with a 30% reduction in mortality seen in the spironolactone group. 2 This effect was only significant in patients with elevated serum levels of collagen synthesis markers, suggesting limitation of excessive extracellular matrix turnover as one mechanism contributing to the beneficial effect of spironolactone. 2

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Effects of glucocorticoids and mineralocorticoids on proliferation and maturation of human peripheral blood stem cells

Cited by 18 publications

References 39 publications

Regulation of Circulating Progenitor Cells in Left Ventricular Dysfunction

Regulation of Circulating Progenitor Cells in Left Ventricular Dysfunction

Correlation of Circulating CD133+ Progenitor Subclasses with a Mild Phenotype in Duchenne Muscular Dystrophy Patients

Aldosterone and d -Glucose Stimulate the Proliferation of Human Cardiac Myofibroblasts In Vitro

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