Influence of ejaculation frequency on seminal parameters.

BACKGROUND: Several factors have been shown to influence semen parameters, one of which is sexual abstinence; a clinical criteria included in the semen evaluation to provide maximum sperm quality. The aim of the present study was to assess the effect of a daily ejaculation frequency on conventional and functional semen parameters. METHODS: Semen samples were collected daily over a period of two weeks of which every second sample per person was processed and analyzed according to the World Health Organization guidelines. Furthermore, mitochondrial function, intracellular reactive oxygen species production and sperm DNA fragmentation were evaluated by flow cytometry. RESULTS: Total sperm count and seminal volume per ejaculation declined and remained decreased for the duration of the daily ejaculation period. However, conventional parameters such as sperm concentration, motility, progressive motility, morphology, vitality and functional parameters such as sperm plasma membrane integrity, mitochondrial membrane potential and DNA fragmentation was not significantly affected and remained similar to the initial measurement throughout the daily ejaculation period. Despite intra- and inter individual variations, the average values of the basic semen parameters remained above the WHO (2010) reference values throughout the daily ejaculation period. Interestingly, a decreasing trend in intracellular ROS production was observed, although statistically not significant. CONCLUSIONS: The study shows that an extended 2 week period of daily ejaculation does not have major clinical effects on conventional and functional seminal parameters.

Exogenous vascular endothelial growth factor supplementation can restore the podocyte barrier-forming capacity disrupted by sera of preeclamptic women.

AIM: To determine whether exogenous vascular endothelial growth factor (VEGF) supplementation to sera from women with preeclampsia can restore the podocyte barrier-forming capacity disrupted after stimulation with sera from these women. MATERIAL AND METHODS: Enzyme-linked immunosorbent assays (ELISAs) for sFlt-1 (soluble VEGF receptor 1) and VEGF were performed in the sera of preeclamptic and healthy pregnant women. VEGF-enriched preeclamptic serum was used to evaluate the capacity of such sera to restore the diminished podocyte barrier capacity secondary to stimulation with untreated preeclamptic sera. RESULTS: Two groups, preeclampsia (n=15) and healthy (n=15) pregnant women, were established. Median serum levels (pg/mL) of sFlt-1 and VEGF were significantly different between groups: 3987 versus 1432 and 6 versus 15.6 (P<0.001). Altered resistance values of podocytes stimulated with sera from women with preeclampsia were recovered after exogenous VEGF supplementation. CONCLUSION: The mean resistance value of cultured podocytes, an indicator of the integrity of the cytoskeleton and the capacity of these cells to form layers, is altered in women with preeclampsia. High levels of sFlt-1, an inhibitor of VEGF observed in high concentrations in the serum of these patients, could be the underlying cause of this alteration. We provide evidence that exogenous VEGF supplementation of the sera of these women could recover this indicator.

Interaction between endothelial cell-derived extracellular vesicles and monocytes: A potential link between vascular thrombosis and pregnancy-related morbidity in antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an autoimmune disease driven by a wide group of autoantibodies primarily directed against phospholipid-binding proteins (antiphospholipid antibodies). APS is defined by two main kinds of clinical manifestations: vascular thrombosis and pregnancy-related morbidity. In recent years, in vitro and in vivo assays, as well as the study of large groups of patients with APS, have led some authors to suggest that obstetric and vascular manifestations of the disease are probably the result of different pathogenic mechanisms. According to this hypothesis, the disease could be differentiated into two parallel entities: Vascular APS and obstetric APS. Thus, vascular APS is understood as an acquired thrombophilia in which a generalised phenomenon of endothelial activation and dysfunction (coupled with a triggering factor) causes thrombosis at any location. In contrast, obstetric APS seems to be due to an inflammatory phenomenon accompanied by trophoblast cell dysfunction. The recent approach to APS raises new issues; for instance, the mechanisms by which a single set of autoantibodies can lead to two different clinical entities are unclear. This review will address the monocyte, a cell with well-known roles in haemostasis and pregnancy, as a potential participant in vascular thrombosis and pregnancy-related morbidity in APS. We will discuss how in a steady state the monocyte-endothelial interaction occurs via extracellular vesicles (EVs), and how antiphospholipid antibodies, by inducing endothelial activation and dysfunction, may disturb this interaction to promote the release of monocyte-targeted procoagulant and inflammatory messages.

Modulation of the activation of endothelial nitric oxide synthase and nitrosative stress biomarkers by aspirin triggered lipoxins: A possible mechanism of action of aspirin in the antiphospholipid syndrome.

PROBLEM: Antiphospholipid syndrome (APS) is characterized by the clinical manifestation of vascular thrombosis (VT) or pregnancy morbidity (PM) and antiphospholipid antibodies (aPL) that can modify the nitric oxide production. Low-dose aspirin is used in the prevention and treatment of diverse alterations of pregnancy. One of the mechanisms of action of aspirin is to induce the production of aspirin-triggered-lipoxins (ATL). The aim of this study was to evaluate the modulatory effect of ATL over the activation of endothelial nitric oxide synthase (eNOS) and nitrosative stress biomarkers induced by aPL. METHODS: We used polyclonal IgG and sera from women with aPL and PM/VT or VT only, and from women with PM only and positive for non-criteria aPL (SN-OAPS). In these sera, biomarkers of nitrosative stress (nitrites and nitrotyrosine) were measured. The protein expression of nitrotyrosine and the phosphorylation of eNOS (at Ser1177) were estimated in human umbilical vein endothelial cells (HUVECs) stimulated with polyclonal IgG with or without ATL. RESULTS: Women with SN-OAPS showed increased circulating levels of nitrites and nitrotyrosine. Likewise, polyclonal IgG from either SN-OAPS or VT patients stimulated nitrotyrosine expression in HUVECs. ATL decreased the nitrotyrosine expression induced by polyclonal IgG from the SN-OAPS group. ATL also recovered the reduced eNOS phosphorylation at Ser1177 in HUVECs stimulated with polyclonal IgG from women with PM/VT or SN-OAPS. CONCLUSIONS: Increased nitrosative stress present in serum of women with SN-OAPS is associated with IgG-mediated impaired endothelial NO synthesis in endothelial cells. ATL prevent these cellular changes.

Effects of anti-beta 2-glycoprotein 1 antibodies and its association with pregnancy-related morbidity in antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by venous, arterial, or small-vessel thrombosis and/or pregnancy-related morbidity, associated with persistent positivity of antiphospholipid antibodies (aPL). Pregnancy-related morbidity in APS patients is characterized by unexplained fetal deaths, premature birth of morphologically normal newborns, and/or consecutive pregnancy losses before the 10th week of gestation. Beta 2-glycoprotein 1 (ß2GP1) is the main antigen recognized by aPL and plays an essential role in the pathogenesis of APS. Antibodies against ß2GP1 (aß2GP1) are involved in damage-generating mechanisms in APS due to their interaction with trophoblasts, decidua, and endothelial cells. aß2GP1 might be used as a prognostic tool for obstetric risk stratification and ß2GP1 could be a target for molecular-targeted treatment to prevent pregnancy morbidity in APS. This review describes these aspects of aß2GP1, including effects on different cellular targets, its association with the severity of obstetric manifestations and the potential of ß2GP1-targeted therapies for APS.

Differences in Endothelial Activation and Dysfunction Induced by Antiphospholipid Antibodies Among Groups of Patients With Thrombotic, Refractory, and Non-refractory Antiphospholipid Syndrome.

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by pregnancy morbidity or thrombosis and persistent antiphospholipid antibodies (aPL) that bind to the endothelium and induce endothelial activation, which is evidenced by the expression of adhesion molecules and the production of reactive oxygen species (ROS) and subsequent endothelial dysfunction marked by a decrease in the synthesis and release of nitric oxide (NO). These endothelial alterations are the key components for the development of severe pathological processes in APS. Patients with APS can be grouped according to the presence of other autoimmune diseases (secondary APS), thrombosis alone (thrombotic APS), pregnancy morbidity (obstetric APS), and refractoriness to conventional treatment regimens (refractory APS). Typically, patients with severe and refractory obstetric APS exhibit thrombosis and are classified as those having primary or secondary APS. The elucidation of the mechanisms underlying these alterations according to the different groups of patients with APS could help establish new therapies, particularly necessary for severe and refractory cases. Therefore, this study aimed to evaluate the differences in endothelial activation and dysfunction induced by aPL between patients with refractory obstetric APS and other APS clinical manifestations. Human umbilical vein endothelial cells (HUVECs) were stimulated with polyclonal immunoglobulin-G (IgG) from different groups of patients n = 21), including those with primary (VTI) and secondary thrombotic APS (VTII) and refractory primary (RI+), refractory secondary (RII+), and non-refractory primary (NR+) obstetric APS. All of them with thrombosis. The expression of adhesion molecules; the production of ROS, NO, vascular endothelial growth factor (VEGF), and endothelin-1; and the generation of microparticles were used to evaluate endothelial activation and dysfunction. VTI IgG induced the expression of adhesion molecules and the generation of microparticles and VEGF. RI+ IgG induced the expression of adhesion molecules and decreased NO production. RII+ IgG increased the production of microparticles, ROS, and endothelin-1 and reduced NO release. NR+ IgG increased the production of microparticles and endothelin-1 and decreased the production of VEGF and NO. These findings reveal differences in endothelial activation and dysfunction among groups of patients with APS, which should be considered in future studies to evaluate new therapies, especially in refractory cases.

Antiphospholipid Antibodies From Women With Pregnancy Morbidity and Vascular Thrombosis Induce Endothelial Mitochondrial Dysfunction, mTOR Activation, and Autophagy.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by thrombosis and pregnancy morbidity (PM) obstetric events together with persistent high titers of circulating antiphospholipid antibodies (aPL). Several mechanisms that explain the development of thrombosis and PM in APS include the association of aPL with alterations in the coagulation cascade and inflammatory events. Other mechanisms disturbing cellular homeostases, such as mitochondrial dysfunction, autophagy, and cell proliferation, have been described in other autoimmune diseases. Therefore, the objective of this study was to investigate the impact of aPL from different patient populations on endothelial cell mitochondrial function, activation of the mammalian target of rapamycin (mTOR) and autophagy pathways, and cellular growth. Using an in vitro model, human umbilical vein endothelial cells (HUVECs) were treated with polyclonal immunoglobulin G (IgG) purified from the serum of women with both PM and vascular thrombosis (PM/VT), with VT only (VT), or with PM and non-criteria aPL (seronegative-obstetric APS, SN-OAPS). We included IgG from women with PM without aPL (PM/aPL-) and healthy women with previous uncomplicated pregnancies (normal human serum, NHS) as control groups. Mitochondrial function, mTOR activation, autophagy, and cell proliferation were evaluated by Western blotting, flow cytometry, and functional assays. IgG from women with PM/VT increased HUVEC mitochondrial hyperpolarization and activation of the mTOR and autophagic pathways, while IgG from patients with VT induced endothelial autophagy and cell proliferation in the absence of elevated mTOR activity or mitochondrial dysfunction. IgG from the SN-OAPS patient group had no effect on any of these HUVEC responses. In conclusion, aPL from women with PM and vascular events induce cellular stress evidenced by mitochondrial hyperpolarization and increased activation of the mTOR and autophagic pathways which may play a role in the pathogenesis of obstetric APS.

Preeclamptic sera directly induce slit-diaphragm protein redistribution and alter podocyte barrier-forming capacity.

BACKGROUND/AIMS: Podocytes are critical in maintaining the filtration barrier of the glomerulus and are dependent on the slit diaphragm. We hypothesized that disturbances of podocyte biology contribute to proteinuria in women with preeclampsia (PE). METHODS: A human podocyte cell line was stimulated with serum from women with PE (patients) and healthy pregnant women (controls); the main changes in 3 important podocyte proteins: podocin, CD2AP and actin were established by immunofluorescence and Western blot; we also searched for changes in cell plasticity by measuring the resistance of cultured podocytes. RESULTS: Different distributions of CD2AP, podocin and actin were observed in the podocytes stimulated with patient sera compared to podocytes stimulated with control sera. We also found that the mean resistance value of podocytes cultured with serum from women with PE was significantly lower than podocytes cultured with serum from controls. There was no difference in the protein expression level of podocin and CD2AP between patients and controls. CONCLUSIONS: We present evidence that there are differences in podocytes when stimulated with sera from women with PE compared to those stimulated with healthy pregnancy sera. This is the first time that podocyte alterations have been directly related to PE; these descriptive findings could be considered as an interesting beginning for further studies relating podocytes and PE.

Mechanisms of Endothelial Dysfunction in Antiphospholipid Syndrome: Association With Clinical Manifestations.

The endothelium is a monolayer of cells that covers the inner surface of blood vessels and its integrity is essential for the maintenance of vascular health. Endothelial dysfunction is a key pathological component of antiphospholipid syndrome (APS). Its systemic complications include thrombotic endocarditis, valvular dysfunction, cerebrovascular occlusions, proliferative nephritis, deep vein thrombosis, and pulmonary embolism. In women, APS is also associated with pregnancy complications (obstetric APS). The conventional treatment regimens for APS are ineffective when the clinical symptoms are severe. Therefore, a better understanding of alterations in the endothelium caused by antiphospholipid antibodies (aPL) may lead to more effective therapies in patients with elevated aPL titers and severe clinical symptoms. Currently, while in vivo analyses of endothelial dysfunction in patients with APS have been reported, most research has been performed using in vitro models with endothelial cells exposed to either patient serum/plasma, monoclonal aPL, or IgGs isolated from patients with APS. These studies have described a reduction in endothelial cell nitric oxide synthesis, the induction of inflammatory and procoagulant phenotypes, an increase in endothelial proliferation, and impairments in vascular remodeling and angiogenesis. Despite these lines of evidence, further research is required to better understand the pathophysiology of endothelial dysfunction in patients with APS. In this review, we have compared the current understanding about the mechanisms of endothelial dysfunction induced by patient-derived aPL under the two main clinical manifestations of APS: thrombosis and gestational complications, either alone or in combination. We also discuss gaps in our current knowledge regarding aPL-induced endothelial dysfunction.

Aspirin: The Mechanism of Action Revisited in the Context of Pregnancy Complications.

Aspirin is one of the most frequently used and cheapest drugs in medicine. It belongs to the non-steroidal anti-inflammatory drugs with a wide range of pharmacological activities, including analgesic, antipyretic, and antiplatelet properties. Currently, it is accepted to prescribe a low dose of aspirin to pregnant women who are at high risk of preeclampsia (PE) because it reduces the onset of this complication. Another pregnancy alteration in which a low dose of aspirin is recommended is the obstetric antiphospholipid syndrome (APS). The most recognized mechanism of action of aspirin is to inhibit the synthesis of prostaglandins but this by itself does not explain the repertoire of anti-inflammatory effects of aspirin. Later, another mechanism was described: the induction of the production of aspirin-triggered lipoxins (ATLs) from arachidonic acid by acetylation of the enzyme cyclooxygenase-2. The availability of a stable analog of ATL has stimulated investigations on the use of this analog and it has been found that, similar to endogenously produced lipoxins, ATL resolves inflammation and acts as antioxidant and immunomodulator. If we consider that in PE and in the obstetric APS, there is an underlying inflammatory process, aspirin might be used based on the induction of ATL. The objective of this review is to revisit the old and new mechanisms of action of aspirin. In particular, it intends to show other potential uses of this drug to prevent certain pregnancy complications in the light of its ability to induce anti-inflammatory and pro-resolving lipid-derived mediators.

Serum Protein Profile in Women With Pregnancy Morbidity Associated With Antiphospholipid Syndrome.

CONTEXT: Antiphospholipid antibodies (aPL) are related with a high risk of pregnancy morbidity (PM) and also of vascular thrombosis. On the basis of recent studies, we expect that in women with PM associated with antiphospholipid syndrome (APS), further factors may be deregulated and involved in pathophysiology of the disease. Such factors may have the potential to become novel biomarkers for APS and its stages. SETTINGS AND DESIGN: Descriptive study from a recurrent pregnancy loss program. AIMS: To study the protein expression in sera from women with PM with or without aPL. MATERIALS AND METHODS: Protein profiles were determined by surface enhanced laser desorption and ionization - time of flight mass spectrometry (SELDI-TOF MS) in the serum samples from women with PM, 10 of them with aPL and 12 without aPL. On the basis of the mass-to-charge ratio (m/z) of the protein, signals differentially expressed between the two groups were compared with data banks to approach candidate proteins. STATISTICAL ANALYSIS USED: To determine the differential expression of each protein, a no paired t-test was performed using Ciphergen Express Client 3.1 software. RESULTS: SELDI-TOF analysis makes it possible to discriminate between several proteins in women with PM with and without aPL, although it does not allow protein identification. Nine proteins were found in significantly higher levels in aPL-positive women. CONCLUSION: The results underline that further factors beyond autoantibodies are involved in PM associated with APS and might lead to the development of new biomarkers.

Modulation of antiphospholipid antibodies-induced trophoblast damage by different drugs used to prevent pregnancy morbidity associated with antiphospholipid syndrome.

PROBLEM: Women with antiphospholipid antibodies (aPLs) present a risk of pregnancy morbidity (PM), vascular thrombosis (VT), or both (PM/VT). aPLs affect trophoblast function, and the aim of this study was to determine the modulation of this aPL-induced damage by different drugs. METHOD OF STUDY: IgG was obtained from women with PM and PM/VT positive to aPLs. Binding of IgG to trophoblastic cells, proliferation, mitochondrial membrane integrity, and trophoblast invasion were assessed. The effect of enoxaparin, aspirin, and aspirin-triggered lipoxin (ATL) were evaluated as well as signal transducer and activator of transcription 3 (STAT3) phosphorylation. RESULTS: IgG from women with aPLs strongly binds to trophoblastic cells. Integrity of mitochondrial membrane was reduced, and proliferation was increased by IgG-PM/VT. Both IgG-PM and IgG-PM/VT decreased trophoblast invasion, which was restored by enoxaparin, aspirin, and ATL. IgG-PM triggered reduction in STAT3 phosphorylation. CONCLUSION: Some drugs used to prevent aPL-induced PM modulated the alteration of trophoblast function.

Physically Active Men Show Better Semen Parameters than Their Sedentary Counterparts.

BACKGROUND: The quality of semen depends upon several factors such as environment, life style, physical activity, age, and occupation. The aim of this study was to analyze and compare the conventional and functional semen parameters in men practicing vigorous physical activity to those of sedentary men. MATERIALS AND METHODS: In this descriptive cross-sectional study, semen samples of 17 physically active men and 15 sedentary men were collected for analysis. Semen analysis was performed according to the World Health Organization (WHO) guidelines, while functional parameters were evaluated by flow cytometry. RESULTS: Results showed that several semen parameters (semen volume, viability, progressive motility, total motility, normal morphology, and moribund cells) were superior in the physically active group in comparison with the sedentary group. Semen parameters such as viability, progressive motility and total motility, as well as the percentage of moribund spermatozoa were significantly different between both groups. However, sperm DNA damage, lipid peroxidation and mitochondrial potential were not significantly different among the groups. CONCLUSION: Nevertheless, the physical activity shows better semen parameters than sedentary group. Taken together, our results demonstrate that regular physical activity has beneficial impact in sperm fertility parameters and such a life style can enhance the fertility status of men.

Aspirin-triggered lipoxin prevents antiphospholipid antibody effects on human trophoblast migration and endothelial cell interactions.

OBJECTIVE: Antiphospholipid antibodies (aPL) interfere with several physiologic functions of human trophoblasts, including reducing their ability to migrate, decreasing their production of angiogenic factors, and inducing an inflammatory response. This may provide the underlying mechanism by which aPL responses lead to recurrent pregnancy loss or preeclampsia in women with obstetric antiphospholipid syndrome (APS). Although treatment with heparin may reduce the rate of recurrent pregnancy loss, the risk of preeclampsia remains high. Therefore, alternative treatments are needed for the management of pregnant patients with APS. Since aspirin-triggered lipoxins (ATLs) have immune and angiogenic modulatory properties, the objective of this study was to determine the effects of the ATL 15-epi-lipoxin A4 on the function of aPL-altered human trophoblasts in the first trimester of pregnancy. METHODS: A first-trimester human trophoblast cell line (HTR8) was treated with mouse anti-human ß2 -glycoprotein I monoclonal antibodies (aPL) in the presence or absence of the ATL 15-epi-lipoxin A4 . Trophoblast migration and interactions with endometrial endothelial cells were measured using Transwell and coculture assays. Trophoblast secretion of cytokines and angiogenic factors was measured by enzyme-linked immunosorbent assay. RESULTS: Treatment of HTR8 cells with ATL reversed the aPL-induced decrease in trophoblast migration, an effect that appeared to be regulated through restoration of interleukin-6 production. Using a model of spiral artery transformation, aPL and sera from APS patients with pregnancy morbidity disrupted trophoblast-endothelial cell interactions, and treatment with ATL restored the stability of the cocultures. In contrast, ATL treatment did not resolve the proinflammatory and antiangiogenic responses of trophoblasts induced by aPL. CONCLUSION: These findings indicate that ATLs may have some benefits in terms of preventing the effects of aPL on trophoblast function, which raises the possibility of the use of ATLs as an adjuvant therapy in women with aPL.

Estrés oxidativo en células endoteliales inducido por el suero de mujeres con diferentes manifestaciones clínicas del síndrome antifosfolípido / Oxidative stress in endothelial cells induced by the serum of women with different clinical manifestations of the antiphospholipid syndrome

Introducción. El síndrome antifosfolípido se caracteriza por la presencia persistente de anticuerpos antifosfolípidos y manifestaciones clínicas de trombosis o morbilidad gestacional, las cuales se asocian con estrés oxidativo y disfunción endotelial. Objetivo. Evaluar los marcadores de estrés oxidativo en células endoteliales, inducidos por el suero de mujeres con diferentes manifestaciones clínicas del síndrome antifosfolípido y analizar la capacidad antioxidante de los sueros. Materiales y métodos. Se incluyeron 48 mujeres que fueron clasificadas así: presencia de anticuerpos antifosfolípidos y criterios clínicos de morbilidad gestacional, trombosis vascular o ambas. Como grupos control se incluyeron mujeres negativas para anticuerpos antifosfolípidos. En un modelo in vitro de células endoteliales estimuladas con los sueros de las mujeres del estudio, se determinaron algunos marcadores de estrés oxidativo por citometría de flujo. También, se analizó la capacidad antioxidante de los sueros incluidos. Resultados. Los sueros de los grupos de mujeres con síndrome antifosfolípido que presentaban trombosis, con morbilidad gestacional o sin ella, generaron un incremento significativo (p<0,05 y p<0,001)en los marcadores de estrés oxidativo endotelial, en contraste con el control de suero humano normal. No se observaron diferencias en el efecto de los sueros de los diferentes grupos de estudio sobre la lipoperoxidación endotelial. Tampoco se encontró diferencia en la actividad antioxidante de los sueros. Conclusión. El estrés oxidativo mitocondrial en el endotelio se asocia con la presencia de trombosis. Sin embargo, cuando esta se asocia con morbilidad gestacional, también se genera estrés oxidativo intracelular.

Introduction: The antiphospholipid syndrome is characterized by the persistent presence of antiphospholipid antibodies and clinical manifestations of thrombosis or gestational morbidity that are associated with oxidative stress and endothelial dysfunction. Objective: To evaluate markers of oxidative stress in endothelial cells induced by the serum from women with different clinical manifestations of the antiphospholipid syndrome, and to analyze the antioxidant capacity of the sera. Materials and methods: We included 48 women who were classified as follows: presence of antiphospholipid antibodies and clinical criteria of gestational morbidity alone, vascular thrombosis only, and gestational morbidity/vascular thrombosis. Control groups included antiphospholipid antibodies negative women. In an in vitro model of endothelial cells stimulated with sera from women included in the groups, some markers of oxidative stress were determined by flow cytometry. The antioxidant capacity in the sera of these women was analyzed. Results: The sera from the groups of women with antiphospholipid syndrome that presented thrombosis, with or without gestational morbidity, generated a significant increase (p<0.05 and p<0.001) in endothelial oxidative stress markers in contrast to the control of normal human serum. There were no differences in the effect of the sera from the different study groups on endothelial lipid peroxidation. Also, there was also no difference in the antioxidant activity of the sera. Conclusion: Mitochondrial oxidative stress in the endothelium is associated with the presence of thrombosis; instead, its association with gestational morbidity generates intracellular oxidative stress.

Remodelación vascular como modelo in vitro para el estudio del síndrome antifosfolipídico obstétrico / Vascular remodeling as in vitro model for the study of the obstetrical antiphospholipid syndrome

Introducción y Objetivo: Los anticuerpos antifosfolípidos (aAFL) se pueden unir a las células trofoblásticas o a las endoteliales, alterando la remodelación vascular y consecuentemente la placentación normal. El objetivo fue evaluar el efecto del suero de pacientes con síndrome antifosfolipídico (SAF) obstétrico en la interacción endotelio-trofoblasto utilizando un modelo in vitro tridimensional de remodelación vascular. Métodos: Las pacientes con aAFL fueron clasificadas en dos grupos: morbilidad gestacional y trombosis (MG/TV, n=7) y morbilidad gestacional sola (MG, n=8). Como control, se incluyeron mujeres sin aAFL con MG (MG/ aAFL-, n=10), y mujeres sanas (SHN, n=7). Células endoteliales HUVEC fueron cultivadas en Matrigel™ hasta formar estructuras tubulares (angiogénesis) y luego se adicionaron células trofoblásticas HTR8; estas células invaden las estructuras tubulares de las células endoteliales mejorando su estabilidad. Se evaluó el efecto de 10% del suero de las mujeres del estudio sobre esta interacción.

Evaluación de estrés nitrosativo y oxidativo en mujeres con diferentes manifestaciones clínicas del síndrome antifosfolipídico / Evaluation of nitrosative stress and oxidative in women with different clinical manifestations of the antiphospholipid syndrome

Introducción:El síndrome antifosfolipídico (SAF) es una enfermedad autoinmune caracterizada por la presencia persistente de anticuerpos antifosfolípidos (aAFL) y manifestaciones clínicas de trombosis y/o morbilidad gestacional que se asocian con estrés nitrosativo/ oxidativo y disminución de la capacidad antioxidante, alterando el desarrollo gestacional. Objetivo: Evaluar algunos biomarcadores de estrés nitrosativo/oxidativo del suero de mujeres con diferentes manifestaciones clínicas del SAF y sus efectos en células endoteliales. Métodos: Se incluyeron sueros de 48 mujeres divididas en dos grupos con y sin aAFL. Se evaluó la concentración de nitritos, la capacidad antioxidante y la actividad de la enzima paraoxonasa