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Dive into the research topics where Eva Cernuda-Morollón is active.

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Featured researches published by Eva Cernuda-Morollón.


Neurology | 2013

Interictal increase of CGRP levels in peripheral blood as a biomarker for chronic migraine

Eva Cernuda-Morollón; Davinia Larrosa; César Ramón; Juan Vega; Pablo Martínez-Camblor; Julio Pascual

Objective: To determine calcitonin gene-related peptide (CGRP) levels outside migraine attacks in peripheral blood as a potential biomarker for chronic migraine (CM). Methods: Women older than 17 years and diagnosed with CM were recruited. Matched healthy women with no headache history and women with episodic migraine (EM) served as control groups, together with a series of patients with episodic cluster headache in a pain-free period. CGRP levels were determined in blood samples obtained from the right antecubital vein by ELISA outside a migraine attack and having taken no symptomatic medication the day before. For ethical reasons, preventatives were not stopped. Results: We assessed plasma samples from 103 women with CM, 31 matched healthy women, 43 matched women with EM, and 14 patients with episodic cluster headache matched for age. CGRP levels were significantly increased in CM (74.90 pg/mL) as compared with control healthy women (33.74 pg/mL), women with EM (46.37 pg/mL), and patients with episodic cluster headache (45.87 pg/mL). Thresholds of 43.45 and 58.22 pg/mL optimize the sensitivity and specificity to differentiate CM from healthy controls and EM, respectively. In the CM group, CGRP levels were significantly increased in women with a history of migraine with aura vs those only experiencing migraine without aura. Variables such as age, analgesic overuse, depression, fibromyalgia, vascular risk factors, history of triptan consumption, or kind of preventative treatment did not significantly influence CGRP levels. Conclusion: Increased CGRP level measured in peripheral blood outside migraine attacks and in the absence of symptomatic medication could be a biomarker helping in the diagnosis of CM.


Headache | 2014

CGRP and VIP Levels as Predictors of Efficacy of Onabotulinumtoxin Type A in Chronic Migraine

Eva Cernuda-Morollón; Pablo Martínez-Camblor; César Ramón; Davinia Larrosa; Esther Serrano-Pertierra; Julio Pascual

Onabotulinumtoxin type A (onabotA) has shown efficacy in chronic migraine (CM). Its precise mechanism of action, however, is unknown.


Pain | 2015

OnabotulinumtoxinA decreases interictal CGRP plasma levels in patients with chronic migraine.

Eva Cernuda-Morollón; César Ramón; Pablo Martínez-Camblor; Esther Serrano-Pertierra; Davinia Larrosa; Julio Pascual

Abstract OnabotulinumtoxinA (onabotA) has shown efficacy in chronic migraine (CM). Its mechanism of action, however, remains obscure. We have analysed whether treatment with onabotA is able to induce changes in interictal plasma calcitonin gene-related peptide (CGRP) concentrations, which have been shown to be increased in patients with CM. Calcitonin gene-related peptide levels were determined in samples obtained from the right antecubital vein using ELISA, outside a migraine attack and having taken no symptomatic medication in the previous 24 hours, in 83 patients with CM (average age 44 years; 94% females) before and 1 month after treatment with 155 to 195 U of onabotA. CGRP levels after onabotA treatment (median, 51.89 pg/mL; range, 199.4-10.2) were significantly lower as compared with CGRP levels obtained before onabotA treatment (median, 74.09 pg/mL; range, 241.0-11.4; P = 0.001). Pretreatment CGRP levels in responders (76.85 pg/mL) were significantly higher than those seen in nonresponders (50.45 pg/mL; P = 0.001). One month after treatment, the CGRP levels did not change in nonresponders (51.89 pg/mL; P not significant), but significantly decreased in responders (52.48 pg/mL; P = 0.003). A number of demographic factors, clinical features, and comorbidities were not different in responders as compared with those of nonresponders. These results confirm that interictal CGRP levels can be of help in predicting the response to onabotA and suggest that the mechanism of action of onabotA in CM is the reversal of sensitization as a result of the inhibition of CGRP release.


PLOS ONE | 2010

Rac activation by the T-cell receptor inhibits T cell migration.

Eva Cernuda-Morollón; Jaime Millán; Mark Shipman; Federica M. Marelli-Berg; Anne J. Ridley

Background T cell migration is essential for immune responses and inflammation. Activation of the T-cell receptor (TCR) triggers a migration stop signal to facilitate interaction with antigen-presenting cells and cell retention at inflammatory sites, but the mechanisms responsible for this effect are not known. Methodology/Principal Findings Migrating T cells are polarized with a lamellipodium at the front and uropod at the rear. Here we show that transient TCR activation induces prolonged inhibition of T-cell migration. TCR pre-activation leads to cells with multiple lamellipodia and lacking a uropod even after removal of the TCR signal. A similar phenotype is induced by expression of constitutively active Rac1, and TCR signaling activates Rac1. TCR signaling acts via Rac to reduce phosphorylation of ezrin/radixin/moesin proteins, which are required for uropod formation, and to increase stathmin phosphorylation, which regulates microtubule stability. T cell polarity and migration is partially restored by inhibiting Rac or by expressing constitutively active moesin. Conclusions/Significance We propose that transient TCR signaling induces sustained inhibition of T cell migration via Rac1, increased stathmin phosphorylation and reduced ERM phosphorylation which act together to inhibit T-cell migratory polarity.


Cephalalgia | 2015

Long-term experience with onabotulinumtoxinA in the treatment of chronic migraine: What happens after one year?

Eva Cernuda-Morollón; César Ramón; Davinia Larrosa; Rocío Alvarez; Nuria Riesco; Julio Pascual

Background OnabotulinumtoxinA (onabotA) has shown its efficacy over placebo in chronic migraine (CM), but clinical trials lasted only up to one year. Objective The objective of this article is to analyse our experience with onabotA treatment of CM, paying special attention to what happens after one year. Patients and methods We reviewed the charts of patients with CM on onabotA. Patients were injected quarterly during the first year but the fifth appointment was delayed to the fourth month to explore the need for further injections. Results We treated 132 CM patients (mean age 47 years; 119 women). A total of 108 (81.8%) showed response during the first year. Adverse events, always transient and mild-moderate, were seen in 19 (14.4%) patients during the first year; two showed frontotemporal muscle atrophy after being treated for more than five years. The mean number of treatments was 7.7 (limits 2–29). Among those 108 patients with treatment longer than one year, 49 (45.4%) worsened prior to the next treatment, which obliged us to return to quarterly injections and injections were stopped in 14: in 10 (9.3%) due to a lack of response and in four due to the disappearance of attacks. In responders, after an average of two years of treatment, consumption of any acute medication was reduced by 53% (62.5% in triptan overusers) and emergency visits decreased 61%. Conclusions Our results confirm the long-term response to onabotA in three-quarters of CM patients. After one year, lack of response occurs in about one out of 10 patients and injections can be delayed, but not stopped, to four months in around 40% of patients. Except for local muscle atrophy in two cases treated more than five years, adverse events are comparable to those already described in short-term clinical trials.


BMC Neuroscience | 2014

Microparticles in multiple sclerosis and clinically isolated syndrome: effect on endothelial barrier function.

Beatriz Marcos-Ramiro; Pedro Oliva Nacarino; Esther Serrano-Pertierra; Miguel Angel Blanco-Gelaz; Babette B. Weksler; Ignacio A. Romero; Pierre Olivier Couraud; Alberto Tuñón; Carlos López-Larrea; Jaime Millán; Eva Cernuda-Morollón

BackgroundCell-derived microparticles are secreted in response to cell damage or dysfunction. Endothelial and platelet dysfunction are thought to contribute to the development of multiple sclerosis (MS). Our aim here is, first, to compare the presence of microparticles of endothelial and platelet origin in plasma from patients with different clinical forms of MS and with clinically isolated syndrome. Second, to investigate the effect of microparticles on endothelial barrier function.ResultsPlatelet-poor plasma from 95 patients (12 with clinically isolated syndrome, 51 relapsing-remitting, 23 secondary progressive, 9 primary progressive) and 49 healthy controls were analyzed for the presence of platelet-derived and endothelium-derived microparticles by flow cytometry. The plasma concentration of platelet-derived and endothelium-derived microparticles increased in all clinical forms of MS and in clinically isolated syndrome versus controls. The response of endothelial barriers to purified microparticles was measured by electric cell-substrate impedance sensing. Microparticles from relapsing-remitting MS patients induced, at equivalent concentrations, a stronger disruption of endothelial barriers than those from healthy donors or from patients with clinically isolated syndrome. MS microparticles acted synergistically with the inflammatory mediator thrombin to disrupt the endothelial barrier function.ConclusionsPlasma microparticles should be considered not only as markers of early stages of MS, but also as pathological factors with the potential to increase endothelial permeability and leukocyte infiltration.


Arteriosclerosis, Thrombosis, and Vascular Biology | 2012

Crosstalk Between Reticular Adherens Junctions and Platelet Endothelial Cell Adhesion Molecule-1 Regulates Endothelial Barrier Function

Laura Fernández-Martín; Beatriz Marcos-Ramiro; Carolina L. Bigarella; Mariona Graupera; Robert J. Cain; Natalia Reglero-Real; Anaïs Jiménez; Eva Cernuda-Morollón; Isabel Correas; Susan Cox; Anne J. Ridley; Jaime Millán

Objective—Endothelial cells provide a barrier between the blood and tissues, which is reduced during inflammation to allow selective passage of molecules and cells. Adherens junctions (AJ) play a central role in regulating this barrier. We aim to investigate the role of a distinctive 3-dimensional reticular network of AJ found in the endothelium. Methods and Results—In endothelial AJ, vascular endothelial-cadherin recruits the cytoplasmic proteins &bgr;-catenin and p120-catenin. &bgr;-catenin binds to &agr;-catenin, which links AJ to actin filaments. AJ are usually described as linear structures along the actin-rich intercellular contacts. Here, we show that these AJ components can also be organized in reticular domains that contain low levels of actin. Reticular AJ are localized in areas where neighboring cells overlap and encompass the cell adhesion receptor platelet endothelial cell adhesion molecule-1 (PECAM-1). Superresolution microscopy revealed that PECAM-1 forms discrete structures distinct from and distributed along AJ, within the voids of reticular domains. Inflammatory tumor necrosis factor-&agr; increases permeability by mechanisms that are independent of actomyosin-mediated tension and remain incompletely understood. Reticular AJ, but not actin-rich linear AJ, were disorganized by tumor necrosis factor-&agr;. This correlated with PECAM-1 dispersal from cell borders. PECAM-1 inhibition with blocking antibodies or small interfering RNA specifically disrupted reticular AJ, leaving linear AJ intact. This disruption recapitulated typical tumor necrosis factor-&agr;–induced alterations of barrier function, including increased &bgr;-catenin phosphorylation, without altering the actomyosin cytoskeleton. Conclusion—We propose that reticular AJ act coordinately with PECAM-1 to maintain endothelial barrier function in regions of low actomyosin-mediated tension. Selective disruption of reticular AJ contributes to permeability increase in response to tumor necrosis factor-&agr;.


Cephalalgia | 2015

Increased VIP levels in peripheral blood outside migraine attacks as a potential biomarker of cranial parasympathetic activation in chronic migraine.

Eva Cernuda-Morollón; Pablo Martínez-Camblor; Rocío Alvarez; Davinia Larrosa; César Ramón; Julio Pascual

Aim The aim of this article is to determine vasoactive intestinal peptide (VIP) levels outside migraine attacks in peripheral blood as a potential biomarker for chronic migraine (CM). Methods Women older than 17 and diagnosed as CM were recruited. Matched healthy women with no headache history and women with episodic migraine (EM) served as control groups, together with a series of patients with episodic cluster headache in a pain-free period. VIP levels were determined in blood samples obtained from the right antecubital vein by ELISA outside a migraine attack, the patients having taken no symptomatic medication the day before. For ethical reasons, preventives were not stopped. Results We assessed plasma samples from 119 women with CM, 33 healthy women, 51 matched women with EM and 18 patients (16 males) with cluster headache matched for age. VIP levels were significantly increased in CM (165.1 pg/ml) as compared to control healthy women (88.5 pg/ml) and episodic cluster headache patients (101.1 pg/ml). VIP levels in EM (134.9 pg/ml) were significantly higher compared to controls and numerically lower than those of CM. Thresholds of 71.8 and 164.5 pg/ml optimized the sensitivity and specificity to differentiate CM from healthy controls and EM, respectively. Variables such as age, CM duration, the presence of aura, analgesic overuse, depression, fibromyalgia, vascular risk factors, history of triptan consumption or kind of preventive treatment did not significantly influence VIP levels. Conclusion Increased interictal VIP level measured in peripheral blood could be a biomarker helping in CM diagnosis, though it does not clearly differentiate between EM and CM.


Journal of Cell Biology | 2016

RhoB controls endothelial barrier recovery by inhibiting Rac1 trafficking to the cell border

Beatriz Marcos-Ramiro; Diego García-Weber; Susana Barroso; Jorge Feito; María C. Ortega; Eva Cernuda-Morollón; Natalia Reglero-Real; Laura Fernández-Martín; Maria C. Durán; Miguel A. Alonso; Isabel Correas; Susan Cox; Anne J. Ridley; Jaime Millán

Rho/ROCK signaling is essential to maintain the integrity of the endothelial barrier, but the contributions of specific Rho GTPase family members are unclear. Here, Marcos-Ramiro et al. show that RhoB specifically regulates intracellular trafficking of the Rho GTPase Rac1 and thereby controls endothelial barrier restoration during inflammation.


Cephalalgia | 2016

Prevalence of cranial autonomic parasympathetic symptoms in chronic migraine: Usefulness of a new scale.

Nuria Riesco; Angel I Pérez-Alvarez; Laura Verano; Carmen García-Cabo; Juana Martínez-Ramos; Pablo Sánchez-Lozano; Eva Cernuda-Morollón; Julio Pascual

Background Cranial autonomic symptoms (CAS) seem to appear in around half of migraine patients. Objective Our aim was to analyse the prevalence and profile of CAS, mainly of cranial autonomic parasympathetic symptoms (CAPS), in a series of patients with chronic migraine (CM) according the new criteria for autonomic symptoms in the current IHS classification. Patients and methods We recruited consecutive CM patients attending our headache clinic. Five CPAS were surveyed: lacrimation, conjunctival injection, eyelid oedema, ear fullness and nasal congestion. They were graded as 0 (absent), 1 (present and mild) and 2 (present and conspicuous); therefore the score in this CAPS scale ranges from 0 to 10 points. As a cranial autonomic sympathetic symptom (CSAS), we also asked about the presence of ptosis. Results We interviewed 100 CM patients. Their mean age was 45 years (18–63 years); 93 were females. Eighteen had no CAPS, while 82 reported at least one CAPS. There were only six patients with scores higher than 5, the mean and median CAPS being 2.1 and 2, respectively. Prevalence of CAPS was lacrimation (49%), conjunctival injection (44%), eyelid oedema (39%), ear fullness (30%) and nasal congestion (20%). Ptosis was reported by 42. Conclusion These results, by using for the first time an easy quantitative scale, confirm that (mild) CAPS are not the exception but the rule in CM patients. The score in this CAPS scale could be of help as a further endpoint in clinical trials or to be correlated with potential biomarkers of parasympathetic activation in primary headaches.

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Jaime Millán

Spanish National Research Council

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Beatriz Marcos-Ramiro

Spanish National Research Council

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Isabel Correas

Spanish National Research Council

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Laura Fernández-Martín

Spanish National Research Council

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Natalia Reglero-Real

Spanish National Research Council

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Miguel A. Alonso

Spanish National Research Council

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Adrián Álvarez-Varela

Spanish National Research Council

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