Impact of depression on circulating endothelial progenitor cells in patients with acute coronary syndromes

Stefano, Rossella Di; Felice, Francesca; Pini, Stefano; Mazzotta, Gianfranco; Bovenzi, Francesco; Bertoli, Daniele; Abelli, Marianna; Borelli, Lucia; Cardini, Alessandra; Lari, Lisa; Gesi, Camilla; Muccignat, Alessandro; Oligeri, Claudia; Michi, Paola; Balbarini, Alberto

doi:10.2459/jcm.0b013e328365c195

Cited by 19 publications

(15 citation statements)

References 40 publications

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“… 15 , 16 , 17 In this regard, there is recent evidence on reduced levels of circulating EPCs in patients with depression and acute coronary syndromes. 18 , 19 Oxidative stress, measured by circulating markers (superoxide dismutase, glutathione, oxLDL, among others) in plasma and platelets, 10 vascular relaxation 20 and animal models, 21 , 22 has been closely associated with major depression. 23 , 24 Studies in a depression model with chronic mild stress rats demonstrated associations between endothelial dysfunction, oxidative stress and depression-like symptoms that were modulated by chronic SSRI.…”

Section: Introductionmentioning

confidence: 99%

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

et al. 2016

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There is a link between depression, cardiovascular events and inflammation. We have explored this connection through endothelial dysfunction, using in vivo and in vitro approaches. We evaluated circulating biomarkers of endothelial dysfunction in patients with major depression at their diagnosis (MD-0) and during antidepressant treatment with the selective serotonin reuptake inhibitor escitalopram, for 8 and 24 weeks (MD-8 and MD-24). Results were always compared with matched healthy controls (CON). We measured in vivo circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs) in blood samples, and assessed plasma levels of soluble von Willebrand factor (VWF) and vascular cell adhesion molecule-1 (VCAM-1). CEC counts, soluble VWF and VCAM-1 were statistically elevated in MD-0 (P<0.01 versus CON) and gradually decreased during treatment. Conversely, EPC levels were lower in MD-0, tending to increase throughout treatment. In vitro studies were performed in human endothelial cells cultured in the presence of sera from each study group. Elevated expression of the inflammation marker intercellular adhesion molecule-1 and oxidative stress, with lower presence of endothelial nitric oxide synthase and higher reactive oxygen species production, were found in cells exposed to MD-0 sera (P<0.05 versus CON). These results were normalized in cells exposed to MD-24 sera. Thrombogenicity of extracellular matrices generated by these cells, measured as expression of VWF, tissue factor and platelet reactivity, showed non-significant differences. We provide a model of cultured endothelial cells reproducing endothelial dysfunction in naive patients with major depression, demonstrating endothelial damage and inflammation at diagnosis, and recovering with selective serotonin reuptake inhibitor treatment for 24 weeks.

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Section: Introductionmentioning

confidence: 99%

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

et al. 2016

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“…Similarly, individuals with anxiety disorders showed a significant lower number of circulating EPCs compared to subjects without mood or anxiety disorders. Cross‐sectional dimensional measurements of depression and anxiety also indicated that high scores at both HAM‐D and HAM‐A were related to depletion of EPCs, corroborating our previous preliminary observations (Di Stefano et al ., ). Overall, our data are in line with those of Dome et al .…”

Section: Discussionmentioning

confidence: 97%

“…Therefore, EPCs may play an important role in the molecular background of depression‐associated cardiovascular morbidity. In a preliminary study, we have shown that major depression decreases EPC levels in ACS patients compared with healthy individuals and patients with current MDE without a history of cardiovascular diseases (Di Stefano et al ., ).…”

Section: Introductionmentioning

confidence: 99%

Influence of depression and anxiety on circulating endothelial progenitor cells in patients with acute coronary syndromes

Felice

Stefano

Pini

et al. 2015

Human Psychopharmacology

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“…LVM refers to the pathological changes in the immune activation state of the body caused by large amounts of cytokines secreted by myocardial cells, under the influence of injury, ventricular wall stress, oxidative stress and partial activation of the neuroendocrine system, which induces myocardial collagen deposition and changes in collagen type and collagen degradation (4). Recent studies on LVM reported the presence of stem cells in the myocardium, which have the ability to differentiate into various cells (5,6). A small number of stem cells are able to express c-kit and nanog surface markers.…”

Section: Introductionmentioning

confidence: 99%

Internal associations and dynamic expression of c-kit and nanog genes in ventricular remodelling induced by adriamycin

Liu

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study aimed to investigate the dynamic expression of the c-kit and nanog genes in rats with left ventricular remodelling induced by adriamycin (ADR), and explore its internal association and mechanism of action. Sprague-Dawley male rats were randomly divided into a normal control group and a heart failure model group. Heart failure was induced by a single intraperitoneal injection of ADR (4 mg/kg) weekly for six weeks. The normal control group was given the same amount of saline. At the eighth week, rat cardiac function was examined to demonstrate the formation of heart failure. The rat hearts were harvested frozen and sectioned, and the expression levels of the nanog and c-kit genes in the myocardial tissue samples were detected using immunohistochemistry, immunofluorescence and reverse transcription-polymerase chain reaction (RT-PCR). Hematoxylin and eosin staining demonstrated various pathological changes in the myocardial cells in the heart failure model group, whereas myocardial infarction was not observed in the normal control group. Immunohistochemistry and immunofluorescence demonstrated that nanog-positive cells were predominantly expressed in the vascular endothelium, with a few myocardial cells and stem cells in normal myocardium. The expression levels of c-kit and nanog in the myocardium of the rats with heart failure decreased significantly. c-kit-positive cells clustered together in the epicardium and its vicinity, and c-kit expression significantly decreased in the myocardium of rats with heart failure, as compared with normal rats. In both groups, some cells co-expressed both the c-kit and nanog genes. The RT-PCR results demonstrated that the expression levels of the two genes in the heart failure model group were significantly lower compared with those in the normal control group (P<0.05).In conclusion, the c-kit-and nanog-positive stem cells decreased in the myocardium of the rats with left ventricular remodelling induced by ADR. Their abnormal expression was significantly correlated with left ventricular remodelling, thereby indicating an internal association (influences of two indexes in the experimental group and control group) between them.

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Impact of depression on circulating endothelial progenitor cells in patients with acute coronary syndromes

Cited by 19 publications

References 40 publications

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

Influence of depression and anxiety on circulating endothelial progenitor cells in patients with acute coronary syndromes

Internal associations and dynamic expression of c-kit and nanog genes in ventricular remodelling induced by adriamycin

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