Carles Gil Giró

Carles  Gil Giró

   

 

Carles Gil Giró

Academic Staff

Phone:
+34 935 868 534

Email:
carles.gil@uab.cat

Adress:

Department of Biochemistry and Molecular Biology
Institut de Neurociències
Faculty of Medicine (room M2-115)
Universitat Autònoma de Barcelona (UAB)
Bellaterra Campus 08193-Cerdanyola del Vallés

Area

Thesis number in address


ROLES AND RESPONSIBILITIES

Senior Professor, Faculty of Medicine, Medicine Degree, Physiotherapy Degree and Biomedical Sciences Degree.

Research Tutor, Neuroscience BsC program.

RESEARCH INTERESTS:

As crucial constituents of the biological membranes, lipids have crucial roles the traffic across the plasma membrane and in the starting of intracellular signaling triggered by extracellular modulators. In consequence, lipids have been evolutionally selected targets for pathogens to modulate host cell processes in order to allow their replication and survival.Specialized microdomains in the biological membranes, called lipid rafts, have been clearly involved in triggering signaling from the plasmatic membrane as well as in membrane trafficking, including entry of pathogens or pathogenic proteins into target cells. Thus, given the essential role of rafts in membrane dynamics, we have focused on the involvement of rafts in two neurological pathologies, Multiple Sclerosis (MS) and Schizophrenia (Sch).

 

CURRENT WORK:

1.-Binding of epsilon toxin from Clostridium perfringens to lipid components from rafts and its possible role in the triggering of Multiple Sclerosis.

Multiple sclerosis (MS) is one of the most common neurological diseases in humans, resulting from demyelination of the central nervous system. Although the origin of MS is currently unknown, data support the role of infectious factors (e.g., Herpesvirus among others) which act together with the genetic background of the host. In a recent work, the role of some strains of the anaerobic bacteria Clostridium perfringens as a triggering factor of MS has been hypothesized. Thus, the release of a cytotoxic protein (epsilon toxin, ETX) by C. perfringens would be involved in the death of myelinating cells. Since the possible role of ETX in MS has emerged, we aimed to detect its primary target molecule from the host, mainly focusing on the lipids present in membrane microdomains (also known as lipid rafts), since some of these lipids have been described as primary targets of other clostridial toxins.

 

2.- Evaluation of the role of cholesterol in the function of neurotransmitter receptors involved in schizophrenia.

Schizophrenia is a chronic disorder affecting 1% of the global population. Its symptoms include psychosis, including hallucinations, and cognitive dysfunction, which predominantly includes deficits in attention, executive dysfunction, and memory. Although schizophrenia is a highly disabling disorder, many patients discontinue life-long treatment due to side-effects and limited efficacy. Schizophrenia is treated with a broad class of antipsychotic medications that act as antagonists of dopamine (D2R) and serotonin (5HT2AR) receptors. Antipsychotics are effective in treating positive symptoms but their efficacy against negative and cognitive symptoms is modest. Since the role of the lipidic environment of the receptors is appearing in recent works as important in the receptors action, we are focusing in the role of cholesterol and sphingolipids in schizophrenia-related neurotransmitter receptors. Thus, the main aim of this research line is to explore the possible role of lipids as pharmacological targets in schizophrenia treatment.

See all Carles Gil  publications at PubMed.

  • Candalija A, Cubí R, Ortega A, Aguilera J, and Gil C (2014) Trk receptors need neutral sphingomyelinase activity to promote cell viability. FEBS Letters, 588: 167-174.
  • Cubí R, Matas LA, Pou M, Aguilera J and Gil C (2013) Differential sensitivity to detergents of actin cytoskeleton from nerve endings. Biochimica et Biophysica Acta (Biomembranes) 1828: 2385-2393.
  • Cubí R, Candalija A, Matas LA, Ortega A, Gil C and Aguilera J (2013) Tetanus toxin Hc fragment induces the formation of ceramide platforms and protects neuronal cells against oxidative stress. Plos One 8 (6): e68055.
  • Rodríguez-Asiain A, Ruiz-Babot G, Romero W, Cubí R, Erazo T, Biondi RM, Bayascas JR, Aguilera J, Gómez N, Gil C, Claro E, Lizcano JM  (2011) Brain Specific Kinase-1 BRSK1/SAD-B associates with lipid rafts: modulation of kinase activity by lipid environment. Biochimica et Biophysica Acta (Molecular and Cellular Biology of Lipids). 1811(12):1124-35.
  • Gil C, Falqués A, Sarró E, Cubí R, Blasi J, Aguilera J, Itarte E (2011) Protein kinase CK2 associates to lipid rafts and its pharmacological inhibition enhances neurotransmitter release. FEBS Letters 585: 414-420.
  • Chaïb-Oukadour I, Gil C, Rodríguez-Alvarez J, Ortega A, Aguilera J (2009) Tetanus toxin Hc fragment reduces neuronal MPP+ toxicity. Molecular and Cellular Neuroscience. 41, 297-303.
  • Gil C, Cubí R, Aguilera J (2007) Shedding of the p75NTR neurotrophin receptor is modulated by lipid rafts. FEBS Letters. 581, 1851-1858.
  • Gil C, Cubí R, Blasi J, Aguilera J (2006) Synaptic proteins associate with a sub-set of lipid rafts when isolated from nerve endings at physiological temperature. Biochemical and Biophysical Research Communications. 384, 1334-1342.
  • Gil C, Soler-Jover A, Blasi J, Aguilera J (2005) Synaptic protein and SNARE complexes are localized in lipid rafts from rat brain synaptosomes. Biochemical and Biophysical Research Communications. 329, 117-124.
  • Chaïb-Oukadour I, Gil C, Aguilera J (2004) The C-terminal domain of the heavy chain of tetanus toxin rescues cerebellar granule neurons from apoptotic death: involvement of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways. Journal of Neurochemistry. 90, 1227-1236.
  • Gil C, Chaib-Oukadour I, Aguilera J (2003) C-terminal fragment of tetanus toxin heavy chain activates Akt and MEK/ERK signaling pathways in a Trk receptor-dependent manner in cultured cortical neurons. Biochemical Journal 273: 613-620.
  • Gil C, Najib A, Aguilera J (2003) Serotonin transport is modulated differently by tetanus toxin and growth factors. Neurochemistry International 42: 535-542.       
  • Pelliccioni P, Gil C, Najib A, Sarri E, Picatoste F, Aguilera J (2001) Tetanus toxin modulates serotonin transport in rat-brain neuronal cultures. Journal of Molecular Neuroscience 17: 303-310.
  • Gil C, Chaib-Oukadour I, Blasi J, Aguilera J (2001) Hc fragment (C-terminal portion of the heavy chain) of tetanus toxin activates PKC isoforms and phosphoproteins involved in signal transduction. Biochemical Journal 356: 97-103.
  • Najib A, Pelliccioni P, Gil C, Aguilera J (2000) Serotonin transporter phosphorylation modulated by tetanus toxin. FEBS Letters 486: 136-142.
  • Gil C, Chaib-Oukadour I, Pelliccioni P, Aguilera J (2000) Activation of signal transduction pathways involving trkA, PLCγ-1, PKC isoforms and ERK-1/2 by tetanus toxin. FEBS Letters 481: 177-182.
Institut de Neurociències
Tel: 93 581 3861 / Fax: +34 93 581 3327

Facultat de Medicina. Edifici M-1
Avinguda de Can Domènech - Campus de la UAB · 08193
Bellaterra (Cerdanyola del Vallès) · Barcelona