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Your search keyword '"Maria J. Arranz"' showing total 2 results
Start Over Author "Maria J. Arranz" Publisher nature publishing group
2 results on '"Maria J. Arranz"'

1. Imaging brain inflammation with [11C]PK11195 by PET and induction of the peripheral-type benzodiazepine receptor after transient focal ischemia in rats

Author

Santiago Rojas, Vanessa Gómez, Maria J. Arranz, Deborah Pareto, Abraham Martín, Esther Verdaguer, Joan D. Gispert, Jesús Purroy, Jordi Llop, Anna M. Planas, Olga Millán, and Ángel Chamorro

Subjects
Male, Pathology, medicine.medical_specialty, Blotting, Western, Ischemia, Inflammation, Standardized uptake value, Rats, Sprague-Dawley, Brain ischemia, Lesion, In vivo, Image Processing, Computer-Assisted, medicine, Animals, RNA, Messenger, Receptor, Cerebral Hemorrhage, Focal ischemia, business.industry, Brain, Cerebral Infarction, Binding, Isoquinolines, Receptors, GABA-A, medicine.disease, Benzodiazepine receptor subtypes, Immunohistochemistry, Rats, Neurology, Cerebral ischemia and/or reperfusion, Ischemic Attack, Transient, Positron-Emission Tomography, Reperfusion Injury, Autoradiography, Neurology (clinical), Radiopharmaceuticals, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Ex vivo
Abstract

[11C]PK11195 is used in positron emission tomography (PET) studies for imaging brain inflammation in vivo as it binds to the peripheral-type benzodiazepine receptor (PBR) expressed by reactive glia and macrophages. However, features of the cellular reaction required to induce a positive [11C]PK11195 signal are not well characterized. We performed [11C]PK11195 PET and autoradiography in rats after transient focal cerebral ischemia. We determined [3H]PK11195 binding and PBR expression in brain tissue and examined the lesion with several markers. [ 11C]PK11195 standard uptake value increased at day 4 and grew further at day 7 within the ischemic core. Accordingly, ex vivo [3H]PK11195 binding increased at day 4, and increases further at day 7. The PET signal also augmented in peripheral regions, but to a lesser extent than in the core. Binding in the region surrounding infarction was supported by [ 11C]PK11195 autoradiography at day 7 showing that the radioactive signal extended beyond the infarcted core. Enhanced binding was preceded by increases in PBR mRNA expression in the ipsilateral hemisphere, and a 18-kDa band corresponding to PBR protein was detected. Peripheral-type benzodiazepine receptor immunohistochemistry showed subsets of ameboid microglia/macrophages within the infarcted core showing a distinctive strong PBR expression from day 4. These cells were often located surrounding microhemorrhages. Reactive astrocytes forming a rim surrounding infarction at day 7 also showed some PBR immunostaining. These results show cellular heterogeneity in the level of PBR expression, supporting that PBR is not a simple marker of inflammation, and that the extent of [11C]PK11195 binding depends on intrinsic features of the inflammatory cells. © 2007 ISCBFM All rights reserved., This work was supported by grants from the Comisión Interministerial de Ciencia y Tecnología (CICYT SAF2005-05793-CO2-01), Fondo de Investigaciones Sanitarias (FIS 2004-1104-O and PI051804-Red IM3), the European Network of Excellence DiMI (LSHB-CT-2005-512146), and Departament d'Unversitats, Recerca i Societat de la Generalitat de Catalunya – Beatriu de Pinós. AM and SR have PhD fellowships from FIS and Ministerio de Educación y Ciencia, respectively.

Published
2007

2. A genome-wide methylation study reveals X chromosome and childhood trauma methylation alterations associated with borderline personality disorder

Author

María J. Arranz, Cristina Gallego-Fabrega, Ana Martín-Blanco, Joaquim Soler, Matilde Elices, Elisabet Dominguez-Clavé, Juliana Salazar, Daniel Vega, Laia Briones-Buixassa, and Juan Carlos Pascual

Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Abstract Borderline personality disorder (BPD) is a severe and highly prevalent psychiatric disorder, more common in females than in males and with notable differences in presentation between genders. Recent studies have shown that epigenetic modifications such as DNA methylation may modulate gene × environment interactions and impact on neurodevelopment. We conducted an epigenome wide study (Illumina Infinium HumanMethylation450k beadchip) in a group of BPD patients with (N = 49) and without (N = 47) childhood traumas and in a control group (N = 44). Results were confirmed in a replication cohort (N = 293 BPD patients and N = 114 controls) using EpiTYPER assays. Differentially methylated CpG sites were observed in several genes and intragenic regions in the X chromosome (PQBP1, ZNF41, RPL10, cg07810091 and cg24395855) and in chromosome 6 (TAP2). BPD patients showed significantly lower methylation levels in these CpG sites than healthy controls. These differences seemed to be increased by the existence of childhood trauma. Comparisons between BPD patients with childhood trauma and patients and controls without revealed significant differences in four genes (POU5F1, GGT6, TNFRSF13C and FAM113B), none of them in the X chromosome. Gene set enrichment analyses revealed that epigenetic alterations were more frequently found in genes controlling oestrogen regulation, neurogenesis and cell differentiation. These results suggest that epigenetic alterations in the X chromosome and oestrogen-regulation genes may contribute to the development of BPD and explain the differences in presentation between genders. Furthermore, childhood trauma events may modulate the magnitude of the epigenetic alterations contributing to BPD.

Published
2021
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