Grupo de Investigación en Células Gliales
Ref: SGR 2017-1625
Coordinador: Dr. Bernardo Catellano
1) To identify the signals modulating the activation of glial cells in different paradigms.
2) To identify the signaling pathways that may be a putative interaction-target to prevent neurodegeneration and promote regeneration.
3) To identify the presence of antigen presenting cells (APCs) in the CNS under both normal and pathological conditions.
4) To identify the signals involved in regulating the inflammatory and immune responses in the CNS.
Líneas de investigación
1) Study of differential signalling and molecular mechanisms involved in modulating the activation, proliferation and glial cell death in different experimental models of innate and acquired immunity: excitotoxic injury, facial nerve axotomy, deafferentation of the dentate fascia of the hippocampus, induction experimental autoimmune encephalopathy (EAE), etc.
2) Characterization of the putative involvement of glial cells in the modulation of the inflammatory and immune responses. We are especially interested in studying the regulation exerted by microglial cells, macrophages and dendritic cells in the regulation of the infiltration, activation, proliferation, anergy and apoptosis of lymphocytes. These studies were developed in Lewis rats and in transgenic mice that over-express inflammatory (IL6) and anti-inflammatory (IL10) cytokines.
3) Study of changes in the expression of extracellular matrix molecules and their cellular receptors, integrins in neurons and glial cells in different paradigms of brain damage including exctotoxicity, axotomy and EAE in normal rats and mice, as well as in transgenic mice over-expressing IL6 and IL10.
4) Interaction with the mechanisms that regulate CNS expression of enzymes and inflammatory cytokines from glial origin through the use of drugs that inhibit the transcription factors involved in the activation of microglia and astroglia, in order to reduce secondary neuronal death subsequent to experimental injury.
5) Evaluation of the possible use of molecular complexes from non-viral origin as vectors in gene therapy strategies to promote neuroprotection.
· Almolda B, Villacampa N, Manders P, Hidalgo J, Campbell IL, González B and Castellano B. Effects of astrocyte-targeted production of interleukin-6 in the mouse on the host response to nerve injury. Glia, 62: 1142- 1161 (2014)
· Almolda B., González B. and B. Castellano. Microglia detection by enzymatic histochemistry. Methods Mol Biol 1041: 243-59 (2013)
· Gonzalez P., Peluffo H., Acarin L., Villaverde A., Gonzalez B. and Castellano B. Interleukin-10 overexpression does not synergize with the neuroprotective action of RGD-containing vectors after postnatal brain excitotoxicity but modulates the main inflammatory cell responses. J Neurosci Res. 90:143-59 (2012)
· Almolda B., Costa M., Montoya M., González B. and Castellano B. Increase in Th17 and T-reg lymphocytes and decrease of IL22 correlate with the recovery phase of acute EAE in rat. PLoS One, 2011;6(11):e27473. (2011)
· Almolda B., González B. and Castellano B. Antigen presentation in EAE: role of microglia, macrophages and dendritic cells. Frontiers in Biosciences, 16:1157-71, Review (2011)