Nifedipine improves the migratory ability of circulating endothelial progenitor cells depending on manganese superoxide dismutase upregulation

Passacquale, Gabriella; Desideri, Giovambattista; Croce, Giuseppe; Murgo, Simona; Mancarelli, Maria Michela; Zazzeroni, Francesca; Alesse, Edoardo; Ferri, Claudio

doi:10.1097/hjh.0b013e3282f4d1bd

Cited by 14 publications

(7 citation statements)

References 40 publications

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“…Furthermore, nifedipine treatment of EPCs cultured from the blood of healthy subjects promoted EPC cell mobility and adhesion to endothelial cells, at least partly by upregulation of manganese superoxide dismutase. Blocking this enzyme by RNA interference abrogated the effect of nifedipine on EPC mobility, suggesting that the positive effects of nifedipine on EPC function probably resulted from increased oxidative stress resistance of the cultured cells [104]. In patients with essential hypertension also nisoldipine was shown to enhance EPC numbers and colony-forming capacity [105].…”

Section: Calcium Antagonistsmentioning

confidence: 97%

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Everaert¹,

Craenenbroeck²,

Hoymans³

et al. 2010

International Journal of Cardiology

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Section: Calcium Antagonistsmentioning

confidence: 97%

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Everaert¹,

Craenenbroeck²,

Hoymans³

et al. 2010

International Journal of Cardiology

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“…Marrotte recently reported that EPCs-mediated augmentation of angiogenesis and wound repair are functionally impaired in diabetes due to decreased SOD2 expression in EPCs, which is restored by SOD2 gene therapy (154). Dihydropyridine calcium antagonist, which reduces cardiovascular events, improves migratory ability of circulating EPCs via upregulation of SOD2 (186). Taken together, SODs in BM-derived stem/ progenitor cells and EPCs play an important role in protecting against oxidative stress, which appears to be an important for their normal function.…”

Section: Sods and Stem Cells/progenitor Cells Functionmentioning

confidence: 99%

Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases

Fukai

Ushio‐Fukai

2011

Antioxidants & Redox Signaling

1,608

1,099

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Excessive reactive oxygen species Revised abstract, especially superoxide anion (O 2 -), play important roles in the pathogenesis of many cardiovascular diseases, including hypertension and atherosclerosis. Superoxide dismutases (SODs) are the major antioxidant defense systems against O 2 -, which consist of three isoforms of SOD in mammals: the cytoplasmic Cu/ZnSOD (SOD1), the mitochondrial MnSOD (SOD2), and the extracellular Cu/ZnSOD (SOD3), all of which require catalytic metal (Cu or Mn) for their activation. Recent evidence suggests that in each subcellular location, SODs catalyze the conversion of O 2 -H 2 O 2 , which may participate in cell signaling. In addition, SODs play a critical role in inhibiting oxidative inactivation of nitric oxide, thereby preventing peroxynitrite formation and endothelial and mitochondrial dysfunction. The importance of each SOD isoform is further illustrated by studies from the use of genetically altered mice and viral-mediated gene transfer. Given the essential role of SODs in cardiovascular disease, the concept of antioxidant therapies, that is, reinforcement of endogenous antioxidant defenses to more effectively protect against oxidative stress, is of substantial interest. However, the clinical evidence remains controversial. In this review, we will update the role of each SOD in vascular biologies, physiologies, and pathophysiologies such as atherosclerosis, hypertension, and angiogenesis. Because of the importance of metal cofactors in the activity of SODs, we will also discuss how each SOD obtains catalytic metal in the active sites. Finally, we will discuss the development of future SODdependent therapeutic strategies. Antioxid. Redox Signal. 15, 1583-1606.

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“…Nifedipine and methyldopa showed a more pronounced effect on restoring EPC colony formation and migration capacities than metoprolol. A previous study has shown that in vitro nifedipine treatment increased the migratory ability of EPCs isolated from healthy donors, depending on manganese superoxide dismutase upregulation . Nifedipine also improved EPC angiogenesis‐related functions, counts and functions in patients with stage 1 hypertension by suppressing EPC apoptosis, and reducing oxidative stress .…”

Section: Discussionmentioning

confidence: 90%

Effects of metoprolol, methyldopa, and nifedipine on endothelial progenitor cells in patients with gestational hypertension and preeclampsia

Yan-gui

Liu

et al. 2019

Clin Exp Pharma Physio

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Hypertension is the most common pathological symptom during pregnancy, occurring in approximately 10% of all pregnancies. 1 As suggested by the American College of Obstetricians and Gynaecologists (ACOG), hypertensive disorders of pregnancy (HDPs) are classified into five categories: (a) chronic hypertension, (b) gestational hypertension, (c) preeclampsia, (d) eclampsia, and (e) preeclampsia superimposed on chronic hypertension. 1,2 Statistically, HDPs feature among the top six causes of maternal mortality in the United States Summary Endothelial progenitor cells (EPCs) are critical for vascular regeneration and function, but are reduced in hypertensive disorders of pregnancy. We aimed to determine the possible effects of antihypertensive drugs, such as metoprolol, methyldopa, and nifedipine, on EPC number and functions in patients with gestational hypertension and preeclampsia. We collected blood samples from 30 normal pregnant women, 67 patients with gestational hypertension and 48 patients with preeclampsia. The patients received no drug or an antihypertensive drug, such as metoprolol, methyldopa, or nifedipine, between 20 and 24 weeks of gestation. The number of EPCs and circulating endothelial cells (CECs) in the blood was measured by flow cytometry. Moreover, colony formation and migration assays were performed on the isolated EPCs. Both the systolic and diastolic blood pressure (BP) increased, while the percentage of flow-mediated vasodilatation (FMD) decreased in patients with gestational hypertension and preeclampsia, compared to the healthy controls at 20 weeks of gestation. CEC number increased in the patients, whereas EPC counts decreased.Furthermore, EPC colony formation and migration abilities were also impaired in the patients. However, administration of metoprolol, methyldopa, or nifedipine effectively restored the systolic and diastolic BP, FMD%, EPCs, and CEC numbers, as well as EPC migration capacity. Endothelial progenitor cells colony formation ability selectively improved with methyldopa and nifedipine. In patients receiving no drugs, most of these indexes worsened within 4 weeks (study duration). This study revealed a new pharmacological action of these antihypertensive drugs against gestational hypertension and preeclampsia, thus supporting their clinical use. K E Y W O R D Santihypertensive drugs, endothelial progenitor cells, gestational hypertension, preeclampsia

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Nifedipine improves the migratory ability of circulating endothelial progenitor cells depending on manganese superoxide dismutase upregulation

Abstract: Nifedipine improves EPC motility due to MnSOD upregulation. The capability of this dihydropyridine calcium antagonist to reduce cardiovascular events might also be related to improved EPC function.

Cited by 14 publications

References 40 publications

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Current perspective of pathophysiological and interventional effects on endothelial progenitor cell biology: Focus on Pi3K/AKT/eNOS pathway

Superoxide Dismutases: Role in Redox Signaling, Vascular Function, and Diseases

Effects of metoprolol, methyldopa, and nifedipine on endothelial progenitor cells in patients with gestational hypertension and preeclampsia

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