Research areas
Cell therapy.
This group carries out research on the use of cell therapy
in neurodegenerative diseases. The main objective of this line of
work is to study the beneficial effects of carotid body transplants
in animal models of Parkinson's disease. Different models of
Parkinson's disease in rats and mice are used, and a range of cell
types have been tested. An important aspect of this area is the
study of the trophic action of transplants, and of the trophic
factors implicated. The group also participates in studies with
patients aimed at possible clinical applications of discoveries
made in the laboratory. To this extent, the group maintains close
collaborative links with other IBIS groups.
Aquaporins.
The group also maintains a line of research aimed at
exploring the physiology of aquaporins, from the study of their
molecular characteristics and the regulation of their genetic
expression, to possible novel functions of these membrane proteins,
with particular emphasis on their role in different pathologies.
Specifically, the regulation by hypoxia of the genetic expression
of aquaporins, and the role these proteins play as gas channels are
under investigation. Concerning the latter, the physiopathological
role of different aquaporins in pulmonary diseases and tumor
processes is being studied. In relation to this research line,
which is being led by Dr. Echevarría, collaborations with other
IBIS groups and various clinical services within HUVR have been
established.
Sanchez-Guijo, F; Garcia-Olmo, D; Prosper, F; Martinez, S; Zapata, A; Fernandez-Aviles, F; Toledo-Aral, JJ; Torres, M; Farinas, I; Badimon, L; Labandeira-Garcia, JL; Garcia-Sancho, J; Moraleda, JM
Spanish Cell Therapy Network (TerCel): 15 years of successful collaborative translational research
CYTOTHERAPY
García-García A, Korn C, García-Fernández M, Domingues O, Villadiego J, Martín-Pérez D, Isern J, Bejarano-García JA, Zimmer J, Pérez-Simón JA, Toledo-Aral JJ, Michel T, Airaksinen MS, Méndez-Ferrer S
Dual cholinergic signals regulate daily migration of hematopoietic stem cells and leukocytes.
Blood.
Trillo-Contreras JL, Toledo-Aral JJ, Echevarría M, Villadiego J
AQP1 and AQP4 Contribution to Cerebrospinal Fluid Homeostasis.
Cells.
Narváez-Moreno B, Sendín-Martín M, Jiménez-Thomas G, Sánchez-Silva R, Suárez-Luna N, Echevarría M, Bernabeu-Wittel J
Expression patterns of aquaporin 1 in vascular tumours.
Eur J Dermatol.
Osorio G, Zulueta-Dorado T, González-Rodríguez P, Bernabéu-Wittel J, Conejo-Mir J, Ramírez-Lorca R, Echevarría M
Expression Pattern of Aquaporin 1 and Aquaporin 3 in Melanocytic and Nonmelanocytic Skin Tumors.
Am J Clin Pathol.
Villadiego J, Romo-Madero S, García-Swinburn R, Suárez-Luna N, Bermejo-Navas A, Echevarría M, Toledo-Aral JJ.
Long-term immunosuppression for CNS mouse xenotransplantation: Effects on nigrostriatal neurodegeneration and neuroprotective carotid body cell therapy.
Xenotransplantation.
Villadiego J, Labrador-Garrido A, Franco JM, Leal-Lasarte M, De Genst EJ, Dobson CM, Pozo D, Toledo-Aral JJ, Roodveldt C.
Immunization with α-synuclein/Grp94 reshapes peripheral immunity and suppresses microgliosis in a chronic Parkinsonism model.
Glia.
Pérez-Villalba A, Sirerol-Piquer MS, Belenguer G, Soriano-Cantón R, Muñoz-Manchado AB, Villadiego J, Alarcón-Arís D, Soria FN, Dehay B, Bezard E, Vila M, Bortolozzi A, Toledo-Aral JJ, Pérez-Sánchez F, Fariñas I.
Synaptic Regulator α-Synuclein in Dopaminergic Fibers Is Essentially Required for the Maintenance of Subependymal Neural Stem Cells.
J Neurosci.
Di Somma A, Cancela Caro P, Blanco MO, Somma T, López-González A, Campero A, Emmerich J, Márquez-Rivas J.
Modified "Extended" Suboccipital Subtonsillar Clipping of a Ruptured Proximal Pica Aneurysm: Technical Note with Relevant Anatomical Demonstration.
World Neurosurg
Galán-Cobo A, Arellano-Orden E, Sánchez Silva R, López-Campos JL, Gutiérrez Rivera C, Gómez Izquierdo L, Suárez-Luna N, Molina-Molina M, Rodríguez Portal JA, Echevarría M.
The Expression of AQP1 IS Modified in Lung of Patients With Idiopathic Pulmonary Fibrosis: Addressing a Possible New Target
Front Mol Biosci.
Trillo-Contreras JL, Ramírez-Lorca R, Hiraldo-González L, Sánchez-Gomar I, Galán-Cobo A, Suárez-Luna N, Sánchez de Rojas-de Pedro E, Toledo-Aral JJ, Villadiego J, Echevarría M.
Combined effects of aquaporin-4 and hypoxia produce age-related hydrocephalus
Biochimica et biophysica acta. Biochim Biophys Acta Mol Basis Dis.
García-Miranda P, Morón-Civanto FJ, Martínez-Olivo MDM, Suárez-Luna N, Ramírez-Lorca R, Lebrato-Hernández L, Lamas-Pérez R, Navarro G, Abril-Jaramillo J, García-Sánchez MI, Casado-Chocán JL, Uclés-Sánchez AJ, Romera M, Echevarría M, Díaz-Sánchez M
Predictive Value of Serum Antibodies and Point Mutations of AQP4, AQP1 and MOG in A Cohort of Spanish Patients with Neuromyelitis Optica Spectrum Disorders.
Int J Mol Sci.
News
RETOS-COLABORACIÓN 2015 – TOLEDO ARAL, JUAN JOSÉ RTC-2015-3309-1 financiado por MINISTERIO DE ECONOMÍA Y COMPETITIVIDAD

Título: “Desarrollo de una terapia para el tratamiento de variantes genéticas de α-sinucleína en la enfermedad de Parkinson”
El objetivo de este proyecto es el desarrollo de una terapia basada en el compuesto NLF-PD-1233 (de nLife), dirigido a los pacientes con enfermedad de Parkinson que presentan alteraciones en la expresión del gen de la alfa-sinucleína.
La selección de pacientes en función de sus variantes génicas permitirá normalizar la población en estudio y obtener una mayor fortaleza en los estudios de identificación de nuevos biomarcadores.
Para la búsqueda de biomarcadores se evaluará la eficacia del tratamiento con NLF-PD-1233 en un modelo in-vitro de progresión de la enfermedad en células IPCs de pacientes que presentan estas alteraciones del gen SNCA. Por otra parte, el consorcio estudiará biomarcadores subrogados al tratamiento con NLF-PD-1233 asociados a neuroinflamación, neurodegeneración, medidas de viabilidad celular, función neuronal, microPET y estudios de comportamiento, en modelos in-vitro, in-vivo y en un modelo de administración crónica de MPTP en ratones transgénicos que presentan duplicación o triplicación del gen SNCA y las mutaciones puntuales del SNCA más abundantes.