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David Andrés González Figueroa

Investigador postdoctoral

Institut des Neurosciences de Montpellier (INM)

Montpellier, Francia

- Enfermedades neurodegenerativas. - Sistema nervioso periférico y músculo esquelético. - Factores pro-fibróticos y matriz extracelular. - Dinámica de Neurofilamentos y su relación con enfermedades neurodegenerativas.

Doctor en Ciencias Biológicas con mención en Biología Celular y Molecular, PONTIFICIA UNIVERSIDAD CATOLICA DE CHILE. Chile, 2018
Licenciatura en Bioquímica, UNIVERSIDAD ANDRES BELLO. Chile, 2010
Magíster en Ciencias Biológicas, PONTIFICIA UNIVERSIDAD CATOLICA DE CHILE. Chile, 2014
Magíster en Bioquímica, UNIVERSIDAD ANDRES BELLO. Chile, 2015
Bioquímico , UNIVERSIDAD ANDRES BELLO. Chile, 2015

Tesista de pregrado Full Time

UNIVERSIDAD ANDRES BELLO

Facultad de Ciencias de la Vida

Santiago, Chile

2012 - 2012
Tesista de doctorado Full Time

PONTIFICIA UNIVERSIDAD CATOLICA DE CHILE

Facultad de Ciencias Biológicas

Santiago, Chile

2013 - 2018
Investigador Postdoctoral Full Time

Institut des Neurosciences de Montpellier

Montpellier, Francia

2018 - A la fecha

Beca Nacional de Doctorado 2013

COMISION NACIONAL DE INVESTIGACION CIENTIFICA Y TECNOLOGICA

Chile, 2013

Beca otorgada por Conicyt para realizar el programa de Doctorado en Ciencias Biologicas con mencion en Biologia Celular y Molecular de la Pontificia Universidad Catolica de Chile
Mejor Admisión al programa de Doctorado

PONTIFICIA UNIVERSIDAD CATOLICA DE CHILE

Chile, 2013

Mejor admisión al programa de Doctorado en Ciencias Biologicas con mencion en Biologia Celular y Molecular del ano 2013. 1er lugar dentro de 15 candidatos
Beca Eventos y Cursos Cortos

COMISION NACIONAL DE INVESTIGACION CIENTIFICA Y TECNOLOGICA

Chile, 2015

Apoyo complementario para asistir a la XIX Reunión Anual de la Sociedad de Biología Celular de Chile
Beca Eventos y Cursos Cortos 2

COMISION NACIONAL DE INVESTIGACION CIENTIFICA Y TECNOLOGICA

Chile, 2016

Beca de apoyo para asistir a la XXX Reunión Anual de la Sociedad de Biología Celular de Chile
Asignación Anual para Gastos Operacionales del Proyecto de Tesis Doctoral

COMISION NACIONAL DE INVESTIGACION CIENTIFICA Y TECNOLOGICA

Chile, 2016

Beca de apoyo para solventar gastos operacionales durante la realización de la tesis doctoral
Beca de Postdoctorado de la AFM-Téléthon

AFM-Téléthon

Francia, 2018

Beca para la realización de un entrenamiento postdoctoral durante 2 años en el Institut des Neurosciences de Montpellier (INM U1051)


Denervation-induced skeletal muscle fibrosis is mediated by CTGF/CCN2 independently of TGF-beta Faundez-Contreras J.; Contreras O.; Vio C.P.; Murphy-Ullrich J.E. Article ISI SCOPUS MATRIX BIOLOGY (2019)
The inhibition of CTGF/CCN2 activity improves muscle and locomotor function in a murine ALS model Rebolledo, DL; Lipson, KE Article ISI SCOPUS HUMAN MOLECULAR GENETICS (2018)
ALS skeletal muscle shows enhanced TGF-beta signaling, fibrosis and induction of fibro/adipogenic progenitor markers Rebolledo, Daniela L.; Asakura, Atsushi Article ISI SCOPUS PLOS ONE (2017)
Reactive oxygen species trigger motoneuron death in non-cell-autonomous models of ALS through activation of c-Abl signaling Fabiola Rojas, David Gonzalez; Nicole Cortes, Estibaliz Ampuero; Diego E. Hernández, Elsa Fritz; Sebastián Abarzua, Alexis Martinez; Alvaro A. Elorza, Alejandra Alvarez; Felipe Court, Brigitte van Zundert Article Frontiers in Cellular Neuroscience (2015)
Mutant SOD1-expressing astrocytes release toxic factors that trigger motoneuron death by inducing hyperexcitability Elsa Fritz, Pamela Izaurieta; Alexandra Weiss, Franco Mir; Patricio Rojas, David González; Fabiola Rojas, Robert H. Brown; Rodolfo Madrid, Brigitte van Zundert Article Journal of Neurophysiology (2013)


Neurofilament aggregation in Charcot-Marie-Tooth diseases: zebrafish as a novel model to study NFs dynamics Bomont P ConferencePoster (2019)
CTGF/CCN2 inhibition improves muscle and locomotor function in an ALS mouse model ConferencePoster (2018)
CTGF/CCN2 activity inhibition reduces fibrosis and improves muscle and locomotor function in an ALS model Lipson K ConferencePoster (2017)
Inhibition of CTGF/CCN2 improves ALS skeletal muscle phenotype and delays disease progression ConferencePoster (2017)
A CTGF neutralizing antibody reduces fibrosis and improves locomotor function in a model of ALS Lipson K ConferencePoster (2016)
CTGF inhibition reduces fibrosis and improves muscle function in a model of ALS Lipson K ConferencePoster (2016)
Denervation-induced fibrosis is modulated by CTGF and HIF-1a Walkinshaw G; Lipson K ConferencePoster (2016)
Denervation-induced fibrosis is modulated by CTGF and HIF-1alpha Walkinshaw G; Lipson K ConferencePoster (2016)
Role of Connective Tissue Growth Factor (CTGF/CCN2) in the fibrosis associated to denervated skeletal muscle and ALS disease progression Lipson K; Walkinshaw G ConferencePoster (2016)
Role of the matricellular protein CTGF/CCN2 in the fibrosis associated to ALS disease Lipson K; Walkinshaw G ConferencePoster (2016)
Study of mutant hSOD1 overexpression in muscles cells and fibroblasts: Evaluation of pro-fibrotic factors expression and ECM deposition Espinoza, JP. ConferencePoster (2016)
Dual Role of HIF-1alpha in damaged skeletal muscle: inducer of angiogenesis and fibrosis Walkinshaw G ConferencePoster (2015)
Fibrosis associated to skeletal muscle denervation and to Amyotrophic Lateral Sclerosis (ALS) model: Role of CTGF/CCN2 Walkinshaw G ConferencePoster (2015)
TGF-b and CTGF pro-fibrotic factors are up-regulated in transgenic ALS model and denervated muscles ConferencePoster (2015)
Astrocytes expressing the ALS-causing mutant SOD1G93A release toxic factor(s) that trigger motoneuron death through activation of c-Abl Cortes N.; Abarzua S.; Ampuero E. ConferencePoster (2014)
CTGF is up-regulated in transgenic SOD1G93A and denervated muscles ConferencePoster (2014)
Modulation of fibrotic markers in skeletal muscle by HIF-1alpha ConferencePoster (2014)
Reduced RECK levels improve the skeletal muscle regeneration and diminish the muscle damage and fibrosis of dystrophic mdx mice ConferencePoster (2014)
TGF-beta signaling pathway is induced in transgenic SOD1G93A fibrotic muscles ConferencePoster (2014)
Astrocytes expressing ALS-causing mutants SOD1 and TDP43 trigger motoneuron death through a common pathogenic pathway involving activation of c-Abl and Nav channels Abarzua S.; Cortes N.; Van Zundert, Brigitte Adriana Johanna ConferencePoster (2013)
RECK a novel matrix-metalloproteinase inhibitor is up-regulated in dystrophic muscles of mdx mice ConferencePoster (2013)
ALS astrocytes release factors that trigger c-Abl phosphorylation in motoneurons: role of sodium channel activity and oxidative stress Abarzua S.; Cortes N. ConferencePoster (2012)
ALS astrocytes release factors that trigger motoneuron death by increasing sodium channel activity Abarzua S.; Cortes N. ConferencePoster (2012)
PSD-95 suppresses dendritic arbor development in mature hippocampal neurons by occluding synapses insertion of NR2B-NMDA receptors Inestrosa, N ConferencePoster (2012)
Epigenetic mechanisms that control PSD95 gene expression in developing hippocampal neurons Bustos, FJ ConferencePoster (2011)