Antonio Felipe Campo  


2006Associate Professor of Biochemistry
and Molecular Biology
Department of Biochemistry and Molecular Biology
University of Barcelona

 

Molecular Physiology Laboratory
Avda. Diagonal 645, 08028 Barcelona, Spain
office:    34-934034616
lab:        34-934039034
fax:        34-934021559
e-mail: afelipe@ub.edu

 




Academic Background Professiosional Experience and Positions Held   Research Interests
Selected Publications  


Academic Background

1984    B.Sc.  (Biology)     University of Barcelona
1985    M.Sc. (Biology)     University of Barcelona
1989    Ph.D.  (Biology)     University of Barcelona
 



Professional Experience and Positions Held

1973-1974     Research Assistant                                                                    INQUIMICA, S.A. (Chemical company)
1974-1985     Research Assistant                                                                    Ferrer Internacional Research Center (Pharmaceutical Company)
1985-1989     Laboratory Head in Biochemical Toxicology                             PRODESFARMA, S.A.   Research Center (Pharmaceutical Company)
1988-1989     Scientific Manager                                                                    PRODESFARMA, S.A. Animal House facilities
1989               Postdoctoral  fellow                                                                  Dept. Biochemistry . University of Bristol , UK ( Dr. J.D.McGivan )
1990-1991     Assistant Professor of Biochemistry and Molecular Biology       Dept. Biochemistry and Physiology, Univ. Barcelona
1991               Research Associate                                                                  Dept. Biochemistry. University of Bristol , UK ( Dr. J.D.McGivan )
1992-1994     Visiting Assistant Professor                                                       Dept. Molecular Physiology and Biophysics , Vanderbilt University , USA ( Dr.M.M. Tamkun )
1991-present  Associate Professor of Biochemistry and Molecular Biology      Dept Biochemistry and Molecular Biology, U. Barcelona



Research Interests

The Molecular Physiology laboratory is interested on the molecular identification and physiological role of  Na and K ionic channels from immune system cells, and its regulation in the cardiovascular and nervous system. Ionic channels are the membrane proteins responsible of the action potential regulation and to keep the membrane potential by passing ions through the lipid structure of plasma membrane. Their activity is very important in synaptic transmission and in the electric waves in the brain. They also play a key role in the cardiac action potential. Whereas the physiological role of ionic channels in tissues having electric properties is quite clear, their role in non-electrically cell types is uncertain. Thus, it has been suggested that ionic channels play an important role in the insulin release from b -pancreatic cells. In kidney are related to ionic reabsortion  and cell volume control during filtering. In uterus, where ionic channels are almost undetectable in basal conditions, are highly induced  the last hours of pregnancy. This fact could be related to the uterine contractions during delivery. In the immune system cells, it is known the existence of Na and K ionic currents however, few proteins have been identified and almost nothing is known about their physiological role. Few studies show that ionic channel activity could be related to nitric oxide production and TNF a release. These results suggest that ionic channels play an important role in the immunological response to external injuries (viral or bacterial infections) or autoimmune diseases. In the striated muscle, ion channels play a key role in cellular differentiation and proliferation. Our interest is to study the role of voltage-dependent ion channels during cell cycle progression and  G0 withdraw. This process leads to myotube fusion by means of membrane hyperpolarization.  The knowledge of the responsible fusion mechanisms between myoblasts and myoubes is important for the treatment based in regeneration and gene therapies in muscle disorders.



Selected Publications

Nucleoside Transport
 

  • Soler, C., Felipe, A., Mata, J.F., Casado, F.J., Celada, A., Pastor-Anglada,M. Regulation of nucleoside transport by lipopolysaccharide, phorbol esters, and tumor necrosis factor   in human B-lymphocytes. J. Biol. Chem. 273 (1998) 26939-26945.
  • Pastor-Anglada, M., Felipe, A.,  and Casado,F.J. Transport and mode of action of nucleoside derivatives used in chemical and antiviral therapies. Trends  in Pharmacological Sciences 19 (1998) 424-430.
  • Soler, C., Felipe, A., Casado, F.J., Celada, A., Pastor-Anglada,M. Nitric oxide regulates nucleoside transport in activated B-lymphocytes. J. Leuk Biol 67 (2000) 345-349.
  • Soler, C., Valdés R., García-Manteiga, J., Xaus, J., Comalada, M., Casado, F.J., Modolell, M., Nicholson, B., Macleod, C., Felipe, A.,  Celada, A., Pastor-Anglada,M. Lipopolisaccharide-induced apoptosis of macrophages determines the up-regulation of concentrative nucleoside transporters Cnt1 and Cnt2 through tumor necrosis factor- a-dependent and -independent mechanisms. J. Biol. Chem. 276 (2001) 30043-30049.
  • Soler, C., García-Manteiga, Valdés R., J., Xaus, J., Comalada, M., Casado, F.J.,  Pastor-Anglada,M., Celada, A., Felipe, A . Macrophages require different nucleoside transport systems for proliferation and activation. FASEB. J. 15 (2001) 1979-198
  • Soler, C., Felipe, A., García-Manteiga, J., Serra, M., Guillen-Gomez, E., Casado, F.J., MacLeod, C., Modolell, M., Pastor-Anglada, M., Celada, A. Interferon -gamma regulates nucleoside transport systems in macrophages through signal transduction and activator of transduction factor 1 (STAT-1)-dependent and independent signalling pathways. Biochem. J. 375 (2003) 777-783.


Ion Channels

  • Felipe, A., Snyders, D.J., Deal, K.K., Tamkun, M.M. Influence of cloned voltage-gated potassium channel expression on alanine transport, Rb+ uptake, and cell volume. American Journal Physiology (Cell Physiology) 265 (1993) C1230-C1238.
  • Felipe, A., Knittle, T.J; Doyle, K.L.; Snyders, D.J.; Tamkun, M.M. Differential expression during development and pregnancy of Isk mRNAs in mouse tissue. American Journal Physiology (Cell Physiology) 267 (1994) C700-C705.
  • Yang, T., Wathen, M.S., Felipe, A., Tamkun, M.M., Snyders, D.J., Roden, D.M. Potassium currents and K+ channel mRNA in cultured atrial cardiac myocytes (AT-1 cells). Circulation Research 75 (1994) 870-878.
  • Felipe, A., Knittle, T.J., Doyle, K.L., Tamkun, M.M. Primary structure and differential expression during development and pregnancy of a novel voltage-gated sodium channel in the mouse. J. Biol. Chem. 269 (1994) 30125-30131.
  • Hulme, J.T., Coppock, E.A, Felipe, A.,  Martens, J.R. and Tamkun, M.M.Oxygen sensitivity of cloned voltage-gated K+ channels expressed in the pulmonary vasculature. Circulation Research 85 (1999) 489-497.
  • Fuster, G., Vicente, R., Coma, M., Grande, M. and Felipe A. One-step reverse transcription polymerase chain reaction for semiquantitative analysis of mRNA expression. Methods Find. Exp. Clin. Pharmacol. 24 (2002) 253-259.
  • Coma, M., Vicente, R., Tsevi, I., Grande, M., Tamkun, M.M. and Felipe A. Different Kv2.1/Kv9.3 heteromer expression during brain and lung post-natal development in the rat. J. Physiol. Biochem. 58 (2002) 195-204.
  • Grande, M., Suarez, E., Vicente, R., Cantó, C., Coma, M., Tamkun, M.M., Zorzano, A., Gumà, A., and Felipe, A. K+ channel b subunits in muscle during postnatal development and myogenesis. Biophys. J. 84 (2003) 235a.
  • Coma, M., Vicente, R., Busquest, S., Carbó, N., Tamkun, M.M., López-Soriano, F.J., Argilés, J.M. and Felipe A. Impaired voltage-gated K+ channel expression in brain during experimental cancer cachexia. FEBS. Lett. 536 (2003) 45-50.
  • Grande, M., Suarez, E., Vicente, R., Cantó, C., Coma, M., Tamkun, M.M., Zorzano, A., Gumà, A., and Felipe, A. Voltage-dependent K+ channel b subunits in muscle: Differential regulation during postnatal development and myogenesis. J. Cell. Physiol. 195 (2003) 187-193.
  • Vicente, R., Escalada, A., Coma, M., Grande, M., Fuster, G., López-Iglesias, C., Solsona, C., and Felipe , A. Voltage-gated potassium channels in macrophages. A journey from proliferation to activation. J. Physiol. 548P (2003) O20. 
  • Vicente, R., Escalada, A., Coma, M., Fuster, G., Sànchez-Tilló, E., López-Iglesias, C., Soler, C., Solsona, C., Celada, A. and Felipe , A. Differential Voltage-dependent K+ channel response during proliferation and activation in macrophages.   J. Biol. Chem. 278 (2003) 46307-46320.
  • Tsevi, I., Vicente, R., Grande M., López-Iglesias, C., Figueras, A., Capellà, G., Condom, E. and Felipe, A. Expression of KCNQ1 and KCNE1 during testis development and germ cell differentiation. Biophys. J. 86 (2004) 126a-127a
  • Vicente, R., Coma, M., Busquets, S., Moore-Carrasco, R., López-Soriano, F.J., Argilés, J.M. and Felipe A. The systemic inflammatory response is involved in the regulation of K+ channel expression in brain via TNF-a-dependent and -independent pathways. FEBS. Lett. 572 (2004) 189-194.
  • Tsevi, I., Vicente, R., Grande M., López-Iglesias, C., Figueras, A., Capellà, G., Condom, E. and Felipe, A. KCNQ1/KCNE1 channels during germ-cell differentiation in the rat: expression associated with testis pathologies. J. Cell. Physiol. 202 (2005) 400-410.
  • Vicente, R., Escalada, A., Soler, C., Grande, M., Celada, A., Tamkun, M.M., Solsona, C. and Felipe , A. Pattern of Kvb subunit expression in macrophages depends upon proliferation and the mode of activation. J. Immunol. 174 (2005) 4736-4744.
  • Felipe, A., Vicente, R.,  Núria Villalonga, N., Roura-Ferrer, M., Martínez-Mármol, R., Solé, L., Ferreres, J.C. and Condom, E. Potassium channels: new targets in cancer therapy. Cancer Detect Prev. 30 (2006) 375-385. 
  • Vicente, R., Escalada, A., Villalonga, N., Texido, L., Roura-Ferrer, M., Martin-Satue, M., Lopez-Iglesias, C., Soler, C., Solsona, C., Tamkun, M.M. and Felipe, A. Association of Kv1.5 and Kv1.3 contributes to the major voltage-dependent  K+ channel in macrophages. J Biol Chem. 281 (2006) 37675-37685.
  • Villalonga N, Escalada A, Vicente R, Sánchez-Tilló E, Celada A, Solsona C, Felipe A. Kv1.3/Kv1.5 heteromeric channels compromise pharmacological responses in macrophages. Biochem Biophys Res Commun. 352 (2007):913-918.
  • Martínez-Mármol R, David M, Sanches R, Roura-Ferrer M, Villalonga N, Sorianello E, Webb SM, Zorzano A, Gumà A, Valenzuela C, Felipe A. Voltage-dependent Na(+) channel phenotype changes in myoblasts. Consequences for cardiac repair. Cardiovasc Res. 76 (2007):430-441.
  • Villalonga N, Ferreres JC, Argilés JM, Condom E, Felipe A. Potassium channels are a new target field in anticancer drug design. Recent Patents Anticancer Drug Discov. 2 (2007):212-223.
  • Vicente R, Villalonga N, Calvo M, Escalada A, Solsona C, Soler C, Tamkun MM, Felipe A. Kv1.5 association modifies Kv1.3 traffic and membrane localization. J Biol Chem. 283 (2008):8756-8764.
  • Villalonga N, Martínez-Mármol R, Roura-Ferrer M, David M, Valenzuela C, Soler C, Felipe A. Cell cycle-dependent expression of Kv1.5 is involved in myoblast proliferation. Biochim Biophys Acta – Mol Cell Res. 1783 (2008):728-736.
  • David M, Martínez-Mármol R, Gonzalez T, Felipe A, Valenzuela C. Differential regulation of Na(v)beta subunits during myogenesis. Biochem Biophys Res Commun. 368 (2008) 761-766.
  • Roura-Ferrer M, Solé L, Martínez-Mármol R, Villalonga N, Felipe A. Skeletal muscle Kv7 (KCNQ) channels in myoblast differentiation and proliferation. Biochem Biophys Res Commun. 369 (2008):1094-1097.


 

 




updated may 2008