Circulating platelet-derived microparticles are elevated in women with polycystic ovary syndrome diagnosed with the 1990 criteria and correlate with serum testosterone levels

Koiou, Ekaterini; Τζιόμαλος, Κωνσταντίνος; Katsikis, Ilias; Kalaitzakis, Emmanouil; Kandaraki, Eleni; Tsourdi, Elena; Delkos, Dimitrios; Papadakis, Efstathios; Panidis, Dimitrios

doi:10.1530/eje-11-0144

Cited by 25 publications

(12 citation statements)

References 32 publications

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“…The parallel assessment of a cohort of KS patients without any treatment could help further refine our results and to distinguish KS‐related from testosterone‐related platelet reactivity alterations. However, the aim of our study was to assess KS subjects under replacement testosterone treatment, with testosterone levels comparable to healthy controls, to exclude the interference of low testosterone levels on platelet reactivity evaluation (Ajayi et al ., ; Koiou et al ., ; Campelo et al ., ). Moreover, some recent data showed that testosterone replacement appeared to have few effects on specific cardiovascular risk factors and on levels of PAI‐1 in KS patients (Pasquali et al ., ; Zitzmann et al ., ).…”

Section: Discussionmentioning

confidence: 98%

Increased platelet reactivity in Klinefelter men: something new to consider

et al. 2015

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SUMMARYPatients with Klinefelter syndrome (KS) exhibit an increased cardiovascular risk, but underlying mechanisms are largely unknown. The present cross-sectional study has been conducted to evaluate platelet reactivity and the expression of platelet activation markers (8-iso-prostaglandin F2a[8-iso-PGF2a] and 11-dehydro-thromboxane-B₂[11-dehydro-TXB2]) in KS patients and healthy controls. Twenty-three consecutive KS patients under testosterone replacement therapy have been included as case group and 46 agematched healthy males recruited among hospital staff served as controls. Light transmission aggregometry was performed in both cases and controls and maximal platelet aggregation (max-A%) was defined as maximal light transmittance reached within 5 min after the addition of 0.2 or 0.4 mM arachidonic acid (AA). A ≥ 50% irreversible light transmittance (LT-50%) following platelet stimulation defined an adequate platelet aggregation and AC-50% was defined as the minimal agonist concentration needed to achieve LT-50%. The AC-50% was 0.26 mM AA for KS and 0.36 mM for controls (p < 0.001). Whereas AA (0.2 mM) induced LT-50% in 69.6% of KS and in 15.2% of controls (p < 0.001), the stimulation with AA (0.4 mM) determined LT-50% in all cases and controls. However, max-A% was higher in KS than in controls both after AA (0.2 mM) (65.61% vs. 46.30%, p = 0.002,) and after AA (0.4 mM) (96.43% vs. 81.04%, p < 0.001). 8-iso-PGF2a and 11-dehydro-TXB2 were higher in KS than in controls (446.54 pg/mg creatinine vs. 230.00 pg/mg creatinine, p < 0.001 and 1278.36 pg/mg creatinine vs. 595.08 pg/mg creatinine, p = 0.001, respectively) and AC-50% inversely correlated with 8-iso-PGF2a (q = À0.548, p < 0.001) and with 11-dehydro-TXB2 (q = À0.523, p < 0.001). In a linear regression model, KS independently predicted a lower AC-50% (b = À0.597, p < 0.001) and higher levels of 8-iso-PGF2a (b = 0.709, p < 0.001) and 11-dehydro-TXB2 (b = 0.605, p < 0.001). In contrast, no correlation has been found between max-A%, testosterone and estradiol levels in KS. We observed increased platelet reactivity in KS. This might, at least in part, explain the increased thrombotic risk associated with this disease.

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Section: Discussionmentioning

confidence: 98%

Increased platelet reactivity in Klinefelter men: something new to consider

et al. 2015

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“…Several studies have now shown that in accordance with these increased risk factors, PCOS patients have increased circulating levels of EVs, particularly pro-coagulant platelet MVs (Koiou et al 2011, Koiou et al 2013. Willis et al (2014) recently measured increased numbers of circulating EVs nearing the exosome size range (!150 nm), with a greater percentage of annexin V Cve MV and 16 miRNA that were differentially expressed compared with matched controls.…”

Section: The Role Of Evs In Diabetes and Metabolic Diseasementioning

confidence: 99%

Microvesicles and exosomes: new players in metabolic and cardiovascular disease

Lawson¹,

Vicencio²,

Yellon³

et al. 2016

Journal of Endocrinology

285

241

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The past decade has witnessed an exponential increase in the number of publications referring to extracellular vesicles (EVs). For many years considered to be extracellular debris, EVs are now seen as novel mediators of endocrine signalling via cell-to-cell communication.With the capability of transferring proteins and nucleic acids from one cell to another, they have become an attractive focus of research for different pathological settings and are now regarded as both mediators and biomarkers of disease including cardio-metabolic disease. They also offer therapeutic potential as signalling agents capable of targeting tissues or cells with specific peptides or miRNAs. In this review, we focus on the role that microvesicles (MVs) and exosomes, the two most studied classes of EV, have in diabetes, cardiovascular disease, endothelial dysfunction, coagulopathies, and polycystic ovary syndrome. We also provide an overview of current developments in MV/exosome isolation techniques from plasma and other fluids, comparing different available commercial and non-commercial methods. We describe different techniques for their optical/biochemical characterization and quantitation. We also review the signalling pathways that exosomes and MVs activate in target cells and provide some insight into their use as biomarkers or potential therapeutic agents. In summary, we give an updated focus on the role that these exciting novel nanoparticles offer for the endocrine community.

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“…Finally, elevations in specific MP populations may be indicative of hormone imbalances. For example, elevations in platelet MPs have been reported in women with polycystic ovary syndrome where they correlate with serum testosterone [143]. In menopausal women, the numbers of platelet, endothelial, monocyte, granulocyte and total MPs are increased with declining oestrogen levels and may be influenced by triacylglycerols (triglycerides) and blood pressure [144,145].…”

Section: Are Mps Reflective Of Disease States?mentioning

confidence: 99%

Microparticles: biomarkers and beyond

et al. 2012

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Membrane microparticles are submicron fragments of membrane shed into extracellular space from cells under conditions of stress/injury. They may be distinguished from other classes of extracellular vesicles (i.e. exosomes) on the basis of size, content and mechanism of formation. Microparticles are found in plasma and other biological fluids from healthy individuals and their levels are altered in various diseases, including diabetes, chronic kidney disease, pre-eclampsia and hypertension among others. Accordingly, they have been considered biomarkers of vascular injury and pro-thrombotic or pro-inflammatory conditions. In addition to this, emerging evidence suggests that microparticles are not simply a consequence of disease, but that they themselves may contribute to pathological processes. Thus microparticles appear to serve as both markers and mediators of pathology. The present review examines the evidence for microparticles as both biomarkers of, and contributors to, the progression of disease. Approaches for the detection of microparticles are summarized and novel concepts relating to the formation of microparticles and their biological effects are examined.

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Circulating platelet-derived microparticles are elevated in women with polycystic ovary syndrome diagnosed with the 1990 criteria and correlate with serum testosterone levels

Cited by 25 publications

References 32 publications

Increased platelet reactivity in Klinefelter men: something new to consider

Increased platelet reactivity in Klinefelter men: something new to consider

Microvesicles and exosomes: new players in metabolic and cardiovascular disease

Microparticles: biomarkers and beyond

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