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23 March 2017
MARCELO GONZLEZ
Research aim
My main interest is focused on elucidating mechanisms regulating vascular tone and deterioration
suffered by these mechanisms when tissues are exposed to conditions that produce oxidative stress in
normal or pathological conditions. My experimental approach seeks to explain pathophysiological
phenomena from molecular and cellular levels. Therefore, our students are training in classical
techniques of vascular physiology (wire myography, placenta perfusion), cell culture (human
endothelium and smooth muscle cells), biophysics (membrane transport), molecular biology (RT
-PCR, qPCR, promoter cloning, transfection), biochemistry (western blot, cell fractionation, etc.).
Actually, one of my objectives is the identification of mechanism and biomarkers for diagnosis and/or
treatment of cardiovascular disease associated with the development of obstetric pathologies such as
gestational diabetes mellitus or preeclampsia. Also my findings can be extrapolates for understanding
chronic diseases with high incidence in world population, such as diabetes mellitus, hypertension and
atherosclerosis.
Associate researchers
Carlos Escudero (U. Biobo), Victoria Gallardo, Claudio Aguayo, Katherina Fernndez, Mara
Mondaca, Marcela Cid (U. Concepcin), Enrique Guzmn-Gutirrez, I Rodrguez (U. San Sebastin),
Marcelo Faras, Luis Sobrevia (P.U. Catlica), Leandro Ziga (U. Talca).
Undergraduate: Astrid Haensgen, Andrea Saavedra, Roberto Villalobos, Carlos Palma, Cristina
Valenzuela (Biochemistry, Faculty of Pharmacy, U. Concepcin), Pamela Careaga, David Gallegos,
Rubn Grandn (Bioengineering, Faculty of Biological Sciences, U. Concepcin).
Research Visitor
UK: Kings College London (2003), University of Manchester (2011). Australia: Baker Research
Institute at U Melbourne (2008).
Publications
Abstracts (with editorial committee and published in ISI journals from 2010)
1. Saavedra A, Rojas S, Gallegos D, Valdivia L, Cid M, Gonzlez M, Faras M. (2015). Role of
endoplasmic reticulum stress in placental vascular dysfunction associated to insulin resistance in
maternal obesity. Placenta, 36; 4: 501-501.
2. Valdivia L, Rojas S, Saavedra A, Gallegos D, Cid M, Faras M, Gonzlez M. (2015). Differential
expression of CHOP and GADD34 in human fetal endothelium from gestational diabetes. Placenta,
36; 4: 504-504.
3. Quezada S, Saavedra A, Valdivia L, Cid M, Gonzlez M. (2015). Differential expression of
catalytic subunits of NADPH oxidase in human placenta from gestational diabetes. Placenta, 36; 4:
505-505.
4. Valenzuela C, vila P, Rojas S, Villalobos R, Palma C, Gallardo V, Sobrevia L, Gonzlez M.
(2013). Effects of acute and long-term incubation with high D-glucose on mechanisms that induces
nitric oxide and reactive oxygen species in human fetal endothelium. Proc 37th IUPS, PCD349.
5. Cabrera L, Rojas S, Gallardo V, Sobrevia L, Wareing M, Gonzlez M. (2012). A role for large
conductance calcium activated potassium channels (BKCa channels) in L-arginine transport and
vasorelaxation induced by insulin in human feto-placental unit. Proc Physiol Soc 27, PC347.
6. Villalobos R, Careaga P, Cabrera L, Palma C, Rojas S, Gallardo V, Gonzlez M. (2012). High D-
glucose increases the NADPH oxidase 2 and 4 mRNA levels and synthesis of reactive oxygen
species involving the activity of PKC and p38MAPK in HUVEC. Proc Physiol Soc 27, PC181.
7. Careaga P, Villalobos R, Palma C, Rojas S, Gallardo V, Gonzlez M. (2012). Oxidative stress
decreases hCAT-1 protein abundance and L-arginine transport in human fetal endothelium. Proc
Physiol Soc 27, C30.
8. Rojas S, Cabrera L, Careaga P, Palma C, Villalobos R, Gallardo V, Sobrevia L, Gonzlez M.
(2011). Insulin reverses the H2O2-induced vasoconstriction in human feto-placental
microcirculation. Proc Physiol Soc 23, PC240.
9. Cabrera L, vila P, Palma C, Nuez M, Gallardo V, Aguayo C, Sobrevia L, Gonzlez M. (2011).
Role of tyrosine kinases activity in vasodilator mechanisms induced by insulin in human fetal vein.
Proc Physiol Soc 23, PC242.
10. Rodrguez N, vila P, Gallardo V, Sobrevia L, Gonzlez M. (2010). Insulin induces hCATs-
dependent relaxation in human umbilical vein. Proc Physiol Soc 19, PC191.
11. vila P, Rojas S, Gallardo V, Sobrevia L, Gonzlez M. (2010). Chronic incubation with high
extracelular D-glucose increase the contractility of human umbilical vein rings. Placenta 31, A-72.
12. Veas C, Gallardo V, Gonzlez M, Lamperti L, Escudero C, Aguayo C. (2010). Umbilical vein
endothelium activation is associated with high maternal levels of E-selectin, VCAM-1 and SFLT-1
in severe pre-eclamptic pregnancies. Placenta 31 A-47.
Previuos grants:
FONDEFIDeA CA12I10374 (CoI) (Chile, 2012-2014). Bio-obtencin de nanopartculas de selenio
encapsuladas en polisacridos para su potencial uso como suplemento alimentario. (w/ M
Mondaca, UdeC).
FONDECYT 11100192 (PI) (2010-2013). Regulation of expression and activity of hCAT-1 by
reactive oxygen species in human endothelium exposed to insulin and high concentrations of
D-glucose.
DIUC 210.033.103-1.0 (PI) (2010/2012). hCATs and NADPH oxidase roles in vascular dysfunction
induced by high extracelular D-glucose in human umbilical vein.
DIUC 211.032.015-1.0 (CoI) (2010/2012). Participacin de Agmatina como Neuromodulador en el
Proceso de Tolerancia y Dependencia de Opiaceos.
CONICYT AT-23070213 (PI) (2007-2009). Transcriptional regulation of SLC7A1by insulin in
human fetal endothelial cells exposed to high extracelular D-glucose: Roles of NF-B, Sp1 and
ROS.
Fields of Specialisation
Vascular function, vascular reactivity, endothelial physiology, membrane transport, diseases of
pregnancy
Research lines
1. Role L-arginine transporters on vascular function
2. Role of insulin as modulator of cardiovascular system
3. Oxidative stress and vascular dysfunction
4. Role of potassium channels in placental vasculature
Contact
Marcelo Gonzlez
Laboratorio de Fisiologa Vascular (LFV)
Department of Physiology
Faculty of Biological Sciences
Universidad de Concepcin
Barrio Universitario s/n, PO Box 160-C, Concepcin 4070386, CHILE.
Web page
http://labfisiovascular.blogspot.cl/
References