Anne Q Reuwer

Amphia Ziekenhui, Breda, North Brabant, Netherlands

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Publications (24)76.36 Total impact

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    ABSTRACT: Antipsychotic drugs have been shown to modulate the expression of ATP-binding cassette transporter A1 (ABCA1), a key factor in the anti-atherogenic reverse cholesterol transport process, in vitro. Here we evaluated the potential of the typical antipsychotic drug haloperidol to modulate the macrophage cholesterol efflux function in vitro and susceptibility to atherosclerosis in vivo. Thioglycollate-elicited peritoneal macrophages were used for in vitro studies. Hyperlipidemic low-density lipoprotein (LDL) receptor knockout mice were implanted with a haloperidol-containing pellet and subsequently fed a Western-type diet for 5 weeks to induce the development of atherosclerotic lesions in vivo. Haloperidol induced a 54% decrease (P=0.043) in the mRNA expression of ABCA1 in peritoneal macrophages. This coincided with a 30% (P<0.001) decrease in the capacity of macrophages to efflux cholesterol to apolipoprotein A1. Haloperidol treatment stimulated the expression of ABCA1 (+51%; P=0.021) and other genes involved in reverse cholesterol transport, i.e. CYP7A1 (+98%; P=0.004) in livers of LDL receptor knockout mice. No change in splenic ABCA1 expression was noted. However, the average atherosclerotic lesion size was significantly smaller (-31%; P=0.039) in the context of a mildly more atherogenic metabolic phenotype upon haloperidol treatment. Importantly, haloperidol markedly lowered MCP-1 expression (-70%; P<0.001) and secretion (-28%; P=0.018) by peritoneal macrophages. These studies show that haloperidol treatment lowers the susceptibility for atherosclerotic lesion development in hyperlipidemic LDL receptor knockout mice. Our findings suggest that the beneficial effect on atherosclerosis susceptibility can be attributed to a haloperidol-induced inhibition of macrophage chemotaxis. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2015 · British Journal of Pharmacology
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    ABSTRACT: The pituitary-derived hormone prolactin has been suggested to stimulate the development of atherosclerosis and cardiovascular disease through its effects on metabolism and inflammation. Here we aimed to challenge the hypothesis that inhibition of prolactin function may beneficially affect atherosclerosis burden. Hereto, atherosclerosis-susceptible low-density lipoprotein (LDL) receptor knockout mice were transplanted with bone marrow from transgenic mice expressing the pure prolactin receptor antagonist Del1-9-G129R-hPRL or their non-transgenic littermates as control. Recipient mice expressing Del1-9-G129R-hPRL exhibited a decrease in plasma cholesterol levels (-29%; P<0.05) upon feeding a Western-type diet, which could be attributed to a marked decrease (-47%; P<0.01) in the amount of cholesteryl esters associated with pro-atherogenic lipoproteins VLDL/LDL. In contrast, Del1-9-G129R-hPRL-expressing mice did not display any change in the susceptibility for atherosclerosis after 12 weeks of WTD feeding. Both the absolute atherosclerotic lesion size (223±33 x 103 m2 for Del1-9-G129R-hPRL vs 259±32 x 103 m2 for controls) and the lesional macrophage and collagen contents were not different between the two groups of bone marrow recipients. Importantly, Del1-9-G129R-hPRL exposure increased levels of circulating neutrophils (+91%; P<0.05), lymphocytes (+55%; P<0.05) and monocytes (+43%; P<0.05), resulting in a 49% higher (P<0.01) total blood leukocyte count. In conclusion, we have shown that prolactin receptor signaling inhibition uncouples the plasma atherogenic index from atherosclerosis susceptibility in LDL receptor knockout mice. Despite an associated decrease in VLDL/LDL-cholesterol levels, application of the prolactin receptor antagonist Del1-9-G129R-hPRL does not alter the susceptibility for initial development of atherosclerotic lesions probably due to the parallel increase in circulating leukocyte concentrations.
    Preview · Article · Jul 2014 · Journal of Endocrinology
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    ABSTRACT: Background Rheumatoid arthritis (RA) mainly affects women. Prolactin (PRL) is a sex hormone with immunomodulatory properties. High prolactin levels are associated with increased disease activity postpartum, and that the PRL-inhibitor bromocriptine improves disease activity of patients with RA. Hyperprolactinemia is observed in 6% of RA-patients, compared to 3% of healthy individuals. The prolactin receptor (PRLR), belonging to the family of cytokine receptors, has been described in atherosclerotic plaques, mainly on macrophages. Objectives The objective of the study is to determine 1) the level of PRL in RA-patients related to treatment effect 2) PRLR expression in synovial tissue of RA, psoriatic arthritis (PsA) and osteoarthritis (OA) patients 3) the phenotype of the PRLR expressing cell. Methods Serum prolactin levels were measured using immunofluorescent metric assay in patients with RA before TNF-α blockade (n=98). The expression of PRLR was determined in synovial tissue (ST) of RA (n=91), PsA (n=15) and OA (n=9) patients using digital image analysis. Immunofluorescence (IF) was used to detect the PRLR expressing cell type. Results Hyperprolactinemia (PRL-level: 16-24 μg/L) was found in 3.8% of the patients with RA. Prolactin levels were highest in premenopausal compared to postmenopausal females and males. Baseline PRL-levels were significantly lower in responders (median (range): 7.0 (2.0-24) μg/L) than in non-responders (9.3 (4.0-19) μg/L)) on TNF treatment (P=0.009). Higher tertiles of PRL (but within the physiological range) were associated with RF-positivity (P=0.005), aCCP-positivity (P=0.06) and erosive disease (P=0.024). After adjustment for these potential confounders, and for baseline-DAS28, baseline-PRL appeared to be a predictor of non-response to anti-TNF treatment (OR: 4.5; P=0.018; table 1). RF and aCCP did not independently contribute. The proportion of patients expressing PRLR in the synovium was similar in RA (66%) and PsA (73%) patients, and lower in OA patients (25%; P=0.05). PRLR expression was higher in RA (median (range): 0.055 (0.000-5.673) IOD/nuclei/mm2) and PsA (0.182 (0.000-5.336)) compared to OA (0.000 (0.000-0.908); P=0.024). Males and (pre-/postmenopausal) females had similar PRLR expression. Using IF, co-localisation was observed with macrophages and endothelial cells. Conclusions Higher levels of PRL independently predicts a non-response to anti-TNF treatment. The expression of the PRLR in synovial tissue, mainly by macrophages, is higher in the inflammatory diseases (RA and PsA) than in OA. Our combined data suggest an important role of prolactin and its receptor in RA. Disclosure of Interest None Declared
    No preview · Article · Jan 2014 · Annals of the Rheumatic Diseases
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    ABSTRACT: Cardiovascular diseases (CVDs) account for approximately 30% of all deaths globally. The most important cause of CVD is atherothrombosis, in other words, narrowing of the arteries as a result of the deposition of cholesterol and other lipoid substances within the arterial wall. Several endocrine disorders have been linked to this pathological state. Recent clinical and experimental studies have suggested that prolactin, a pleiotropic pituitary hormone, may potentially contribute to CVD, either through direct modulation of local cellular processes within atherosclerotic plaques/thrombi and/or through influencing conventional cardiovascular metabolic risk factors. However, the precise role of prolactin in the pathology of CVD remains largely unknown. Here, the authors speculate whether prolactin-lowering treatment may become a future therapeutic approach in patients with elevated prolactin levels and concomitantly presenting with coexisting vascular disease or a significantly elevated risk for premature atherothrombotic vascular disease. Awareness of these new developments may also change our clinical opinions about therapeutic strategies in patients with prolactinomas.
    No preview · Article · Jan 2014 · Expert Review of Endocrinology & Metabolism
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    ABSTRACT: Prolactin is best known as the polypeptide anterior pituitary hormone, which regulates the development of the mammary gland. However, it became clear over the last decade that prolactin contributes to a broad range of pathologies, including breast cancer. Prolactin is also involved in angiogenesis via the release of pro-angiogenic factors by leukocytes and epithelial cells. However, whether prolactin also influences endothelial cells, and whether there are functional consequences of prolactin-induced signalling in the perspective of angiogenesis, remains so far elusive. In the present study, we show that prolactin induces phosphorylation of ERK1/2 and STAT5 and induces tube formation of endothelial cells on Matrigel. These effects are blocked by a specific prolactin receptor antagonist, del1-9-G129R-hPRL. Moreover, in an in vivo model of the chorioallantoic membrane of the chicken embryo, prolactin enhances vessel density and the tortuosity of the vasculature and pillar formation, which are hallmarks of intussusceptive angiogenesis. Interestingly, while prolactin has only little effect on endothelial cell proliferation, it markedly stimulates endothelial cell migration. Again, migration was reverted by del1-9-G129R-hPRL, indicating a direct effect of prolactin on its receptor. Immunohistochemistry and spectral imaging revealed that the prolactin receptor is present in the microvasculature of human breast carcinoma tissue. Altogether, these results suggest that prolactin may directly stimulate angiogenesis, which could be one of the mechanisms by which prolactin contributes to breast cancer progression, thereby providing a potential tool for intervention.
    Full-text · Article · Dec 2011 · Journal of Cellular and Molecular Medicine
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    ABSTRACT: Prolactin is best known as the polypeptide anterior pituitary hormone, which regulates the development of the mammary gland. However, it became clear over the last decade that prolactin contributes to a broad range of pathologies, including breast cancer. Prolactin is also involved in angiogenesis via the release of pro-angiogenic factors by leukocytes and epithelial cells. However, whether prolactin also influences endothelial cells, and whether there are functional consequences of prolactin-induced signalling in the perspec-tive of angiogenesis, remains so far elusive. In the present study, we show that prolactin induces phosphorylation of ERK1/2 and STAT5 and induces tube formation of endothelial cells on Matrigel. These effects are blocked by a specific prolactin receptor antagonist, del1-9-G129R-hPRL. Moreover, in an in vivo model of the chorioallantoic membrane of the chicken embryo, prolactin enhances vessel den-sity and the tortuosity of the vasculature and pillar formation, which are hallmarks of intussusceptive angiogenesis. Interestingly, while prolactin has only little effect on endothelial cell proliferation, it markedly stimulates endothelial cell migration. Again, migration was reverted by del1-9-G129R-hPRL, indicating a direct effect of prolactin on its receptor. Immunohistochemistry and spectral imaging revealed that the prolactin receptor is present in the microvasculature of human breast carcinoma tissue. Altogether, these results sug-gest that prolactin may directly stimulate angiogenesis, which could be one of the mechanisms by which prolactin contributes to breast cancer progression, thereby providing a potential tool for intervention.
    No preview · Dataset · Nov 2011
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    ABSTRACT: Atherothrombosis is a multifactorial process, governed by an interaction between the vessel wall, hemodynamic factors and systemic atherothrombotic risk factors. Recent in vitro, human ex vivo and animal studies have implicated the hormone prolactin as an atherothrombotic mediator. To address this issue, we evaluated the anatomy and function of various microvascular beds as well as plasma atherothrombosis markers in patients with elevated prolactin levels. In this pilot study, involving 10 prolactinoma patients and 10 control subjects, sidestream dark field (SDF) imaging revealed a marked perturbation of the sublingual microcirculation in prolactinoma patients compared to control subjects, as attested to by significant changes in microvascular flow index (2.74 ± 0.12 vs. 2.91 ± 0.05, respectively; P = 0.0006), in heterogeneity index (0.28 [IQR 0.18-0.31] vs. 0.09 [IQR 0.08-0.17], respectively; P = 0.002) and lower proportion of perfused vessels (90 ± 4.0% vs. 95 ± 3.0%, respectively; P = 0.016). In the retina, fluorescein angiography (FAG) confirmed these data, since prolactinoma patients more often have dilatated perifoveal capillaries. In plasma, prolactinoma patients displayed several pro-atherogenic disturbances, including a higher endogenous thrombin potential and prothrombin levels as well as decreased HDL-cholesterol levels. Prolactinoma patients are characterized by microvascular dysfunction as well as plasma markers indicating a pro-atherothrombotic state. Further studies are required to assess if prolactin is causally involved in atherothrombotic disease.
    Full-text · Article · Oct 2011 · Pituitary
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    ABSTRACT: Despite improvement of microvascular outcomes as a consequence of optimal glucose control in patients with type 2 diabetes, prevention of macrovascular complications is still a major challenge. Of interest, large-scale intervention studies (Action to Control Cardiovascular Risk in Diabetes, Action in Diabetes and Vascular Disease-Preterax and Diamicron Modified Release Controlled Evaluation and Veterans Affairs Diabetes Trial) comparing standard therapy versus more intensive glucose-lowering therapy failed to report beneficial impacts on macrovascular outcomes. Consequently, it is currently under debate whether the high doses of exogenous insulin that were administered in these trials to achieve strict target glucose levels could be responsible for these unexpected outcomes. Additionally, a potential role for plasma insulin levels in predicting macrovascular outcomes has emerged in patients with or without type 2 diabetes. These observations, combined with evidence from in vitro and animal experiments, suggest that insulin might have intrinsic atherogenic effects. In this review, we summarize clinical trials, population-based studies as well as data emerging from basic science experiments that point towards the hypothesis that the administration of high insulin doses might not be beneficial in patients with type 2 diabetes and established macrovascular disease.
    No preview · Article · Jul 2011 · Diabetes Obesity and Metabolism
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    ABSTRACT: Objective The aim of this trial was to determine whether obese patients benefit from treatment with rimonabant in terms of progression of carotid atherosclerosis. Rimonabant, a selective cannabinoid-1 receptor blocker, reduces body weight and improves cardiometabolic risk factors in patients who are obese. Design, setting, patients, interventions and results A prospective, double-blind, placebo-controlled trial (Atherosclerosis Underlying Development assessed by Intima–media Thickness in patients On Rimonabant (AUDITOR)) randomised 661 patients with abdominal obesity and metabolic syndrome to rimonabant or placebo for 30 months of treatment. The absolute change in the average value for six segments of far wall carotid intima–media thickness from baseline to month 30 was 0.010±0.095 mm in the rimonabant group and 0.012±0.091 mm in the placebo group (p=0.67). The annualised change was an increase of 0.005±0.042 mm for the rimonabant-treated group and 0.007±0.043 mm for the placebo-treated group (p=0.45). Conclusions There was no difference in atherosclerosis progression between patients receiving rimonabant for 30 months and those receiving placebo for the primary efficacy measure (absolute change in carotid intima–media thickness). These findings are consistent with a similar study using coronary intravascular ultrasound and another study evaluating the occurrence of cardiovascular events. Our findings suggest that a 5% loss of body weight over a 30-month period with rimonabant is insufficient to modify atherosclerosis progression in the carotid artery in obese patients with metabolic syndrome. Clinical trial registration information clinicaltrials.gov Identifier: NCT00228176.
    Full-text · Article · Jul 2011 · Heart (British Cardiac Society)
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    ABSTRACT: The objective of the present study was to evaluate the association between adiponectin levels and incidence of coronary heart disease (CHD). We performed a prospective case-control analysis nested in the EPIC-Norfolk cohort. Participants were apparently healthy men and women 45 to 79 years of age who developed fatal or nonfatal CHD during an average follow-up period of 7.7 ± 1.1 years. In total 1,035 participants with incident CHD were matched for age, gender, and enrollment time to 1,920 controls who remained free of CHD over the study follow-up. Baseline nonfasting plasma adiponectin concentrations were determined by enzyme-linked immunosorbent assay. Adiponectin levels were lower in participants with CHD than in matched controls (men 8.74 vs 9.13 μg/ml, p = 0.01; women 12.6 vs 13.4 μg/ml, p = 0.03). A 1-μg/ml increment in adiponectin was associated with decreased CHD risk (odds ratio 0.78, 95% confidence interval 0.63 to 0.96, p = 0.02, in men; odds ratio 0.73, 95% confidence interval 0.55 to 0.96, p = 0.03, in women). However, this association was no longer significant after adjustment for established cardiovascular risk factors. Stratification of participants according to metabolic syndrome status showed that men and women with metabolic syndrome had a higher CHD risk, irrespective of their adiponectin levels. In conclusion, although a low adiponectin concentration is associated with an increased CHD risk, findings of the present study do not suggest that its measurement is useful to refine CHD risk assessment once traditional risk factors and clinical features of the metabolic syndrome have been considered.
    No preview · Article · May 2011 · The American journal of cardiology
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    ABSTRACT: Several acquired risk factors for venous thrombosis (VT) are associated with high prolactin levels. Our goal was to investigate VT risk for different levels of prolactin. We used data of a case-control study on leg vein thrombosis conducted between September 1999 and August 2006 at the Academic Medical Center, Amsterdam, the Netherlands. Prolactin was assessed in 187 cases (mean age, 57 years; range, 19 to 90) and 374 gender-matched controls (mean age, 57 years; range, 18 to 93). Odds ratios and 95% CI for VT risk were estimated based on several cutoff levels derived from prolactin levels in controls. Odds ratios for VT risk clearly increased with higher prolactin levels. For prolactin levels above the 75th percentile (8 μg/L), we found an odds ratio of 1.7 (95% CI 1.0 to 2.7) as compared with levels below the 50th percentile (6 μg/L). This further increased up to an odds ratio of 4.7 (95% CI 1.8 to 11.8) for prolactin levels above the 97.5th percentile (16 μg/L). The risk was most pronounced in premenopausal women. Our data suggest that prolactin levels are associated with VT in a dose-dependent fashion. Future studies are needed to evaluate the causality of this relationship.
    Full-text · Article · Mar 2011 · Arteriosclerosis Thrombosis and Vascular Biology
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    ABSTRACT: Atherosclerotic vascular disease is the consequence of a chronic inflammatory process, and prolactin has been shown to be a component of the inflammatory response. Additionally, recent studies indicate that prolactin contributes to an atherogenic phenotype. We hypothesized that this may be the result of a direct effect of prolactin on atherogenesis through activation of the prolactin receptor. Human carotid atherosclerotic plaques were obtained from patients by endarteriectomies. The mRNA of prolactin receptor, but not of prolactin, was detected in these atherosclerotic plaques by quantitative real-time PCR. In situ hybridization confirmed the expression of the prolactin receptor in mononuclear cells. Analysis at the protein level using immunohistochemistry and immunoelectron microscopy revealed that the prolactin receptor was abundantly present in macrophages near the lipid core and shoulder regions of the plaques. Our findings demonstrate that the prolactin receptor is present in macrophages of the atherosclerotic plaque at sites of most prominent inflammation. We therefore propose that prolactin receptor signaling contributes to the local inflammatory response within the atherosclerotic plaque and thus to atherogenesis.
    Full-text · Article · Nov 2010 · Journal of Endocrinology
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    ABSTRACT: Prolactin may contribute to an atherogenic phenotype. Furthermore, previous studies have shown that prolactin levels increase in situations of acute stress and inflammation. We therefore aimed to investigate the relationship between prolactin, acute stress and inflammation in patients with myocardial infarction. We performed a case-control study in 40 patients with myocardial infarction and 39 controls, aged 41-84 years. Blood for assessment of prolactin and high sensitive C-reactive protein (hsCRP) was drawn at inclusion, that is, during the acute phase of the event, and 2-3 weeks later. Unexpectedly, prolactin levels at inclusion did not differ between cases and controls (7.0 ng/ml and 6.0 ng/ml, respectively, p=0.28). 2-3 weeks later prolactin levels in cases had not decreased. However, univariate regression analysis indicated that hsCRP is associated with prolactin levels (regression coefficient β 0.11; [95% CI 0.01; 0.21]; p=0.03) in cases during the acute phase of myocardial infarction. Our findings may suggest that prolactin is involved in the systemic inflammatory response, which takes place during myocardial infarction; however, this association may not be strong enough to induce higher prolactin levels in patients with myocardial infarction.
    No preview · Article · Sep 2010 · Hormone and Metabolic Research
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    ABSTRACT: Although peripartum cardiomyopathy (PPCM) is a rare disease, it has very serious consequences for both mother and child. No single cause has been held responsible for the pathogenesis. Recent studies have indicated that increased proteolytic cathepsin D activity in cardiomyocytes results in16kDa prolactin fragments with anti-angiogenic and apoptotic properties, which may contribute to the development of PPCM. In support of these findings, lowering full-length prolactin production by bromocriptine therapy has been reported to prevent impairment of cardiac function. PPCM is associated with an increased co-existence of pre-eclampsia, however, a causal relationship has been disputed. We hypothesize that the pathophysiology of PPCM and pre-eclampsia share the same molecular pathway: increased activity of trophoblastic matrix metalloproteinases at the feto-maternal interface may aggravate proteolysis of full-length prolactin, and subsequently the formed 16kDa prolactin fragments may contribute to deterioration of PPCM and pre-eclampsia. Therefore, we argue that it may be worthwhile to explore wether prolactin inhibition is not only beneficial for PPCM patients, but also for the much more prevalent pre-eclamptic women.
    No preview · Article · Sep 2009 · Medical Hypotheses

  • No preview · Article · Aug 2009
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    ABSTRACT: Prolactin is increasingly recognized to play a stimulatory role in the inflammatory response. Because inflammation is considered of crucial importance in the development of atherosclerosis, we aimed to evaluate whether prolactin levels are associated with the occurrence of coronary artery disease (CAD). We performed a nested case-control study in the prospective EPIC-Norfolk cohort. Cases were apparently healthy men and women, aged 45 to 79 years, who developed fatal or nonfatal CAD (n=882). Controls remained free of CAD (n=1490). Overall, systemic prolactin levels did not differ between cases and controls, and people in the highest prolactin tertile did not have a significantly increased risk of developing future CAD (in men, odds ratio, 1.21; 95% CI, 0.92 to 1.61; in women, odds ratio, 1.12; 95% CI, 0.76 to 1.64). However, in a separate immunohistochemical study, the presence of prolactin receptors could be demonstrated in postmortem human coronary artery plaques (preliminary data). Elevated systemic prolactin levels do not predict CAD in the general population. However, prolactin receptors were found in human coronary artery plaques. This observation may indicate a role of prolactin within atherosclerotic plaques. More studies are needed to define the possible role of prolactin in atherosclerotic plaque development.
    No preview · Article · Aug 2009 · Circulation Cardiovascular Genetics
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    ABSTRACT: Several endocrine disorders have been associated with an increased risk of cardiovascular disease (CVD) and mortality. In addition, even subtle hormonal disturbances may modulate the function of cardiovascular organs. In this article, we discuss in detail the contribution of thyroid hormones, cortisol, the somatotropic hormones, and prolactin in the development of CVD. We do not only discuss epidemiological evidence on the association between hormones and cardiovascular disease, but we also address possible pathophysiological mechanisms underlying this association. In fact, hormones can contribute to the development of CVD both indirectly by inducing secondary metabolic changes such as hypertension, insulin resistance, or dyslipidemia, and directly by modulation of cellular pathways that are important in the process of atherosclerotic plaque formation (atherogenesis), plaque instability, and thrombosis. To date several new therapeutic approaches that focus on the control of hormones at the tissue level, independently of their circulating levels, are being developed. These may offer new possibilities for cardiovascular risk reduction.
    Full-text · Article · Aug 2009 · Seminars in Thrombosis and Hemostasis
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    ABSTRACT: Platelets play an important role in the development of plaque formation and in the events after rupture of the atherosclerotic plaque, leading to atherothrombosis. Multiple hormones, either in excess or when deficient, are involved in the development of atherothrombotic disease, but, to which extent such hormones affect platelet function, is still controversial. It was the objective of this study to assess the ability of the pituitary hormone prolactin to affect platelet functions. Venous blood was collected from six healthy males. Platelet activation was studied by (i) flow cytometry in whole blood (exposure of P-selectin as a measure of platelet secretion, and binding of PAC-1 as a measure of ligand-binding conformation of alpha(IIb)beta(3)), and by (ii) optical aggregation and whole blood aggregation. All studies were performed without and with exposure to several concentrations of ADP (0.1, 0.5 and 1.0 microM) and prolactin (50 and 1,000 microg/l). The presence of the prolactin receptor was investigated by Western blot and flow cytometry. In response to either 50 or 1,000 microg/l prolactin, no evidence of platelet activation or aggregation was found. In addition, ADP-induced platelet activation or aggregation was not enhanced by prolactin. Finally, prolactin receptors could not be detected on the surface of platelets. The present data indicate that prolactin does not directly modulate platelet function.
    Full-text · Article · Jul 2009 · Thrombosis and Haemostasis

  • No preview · Article · Jun 2009 · Atherosclerosis Supplements

  • No preview · Article · Jun 2009 · Atherosclerosis Supplements