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Ana M. Cárdenas

Principal Investigator at Centro Interdisciplinario de Neurociencia de Valparaíso.
Full Professor at Faculty of Sciences, Universidad de Valparaíso.
Chemistry and Pharmacy, Universidad de Chile, 1984
Ph.D. in Pharmacology, Universidad Complutense de Madrid, 1988
Postdoctoral training at National Institutes of Health, USA, 1992-1994

Curriculum Vitae

Contact information:

Pasaje Harrington 287, Playa Ancha. Valparaíso
Phone: (56)-(32)-2508040

Our group studies the molecular mechanisms that control vesicle trafficking and exocytosis in neurons, neuroendocrine cells and myocytes, with a special focused in pathogenic mechanisms involved in neuropathies, myopathies and Down syndrome. To this aim, we use techniques such as amperometry and total internal reflection fluorescence microscope (TIRFM) that enable us to monitor single exocytosis events in real time, in three different types of cells: (1) adrenal chromaffin cells, which release adrenaline, neuropeptides and other chemicals in response to stress, (2) cell lines derived from hippocampus and cerebral cortex of trisomy 16 mice, an animal model of Down syndrome, and (3) a human skeletal muscle cell line.

  • González-Jamett AM, Báez-Matus X, Hevia MA, Guerra MJ, Olivares MJ, Martínez AD, Neely A, Cárdenas AM (2010) The association of dynamin with synaptophysin regulates quantal size and duration of exocytotic events in chromaffin cells. J Neurosci. 30:10683-91.
  • González-Jamett AM, Momboisse F, Guerra MJ, Ory S, Báez-Matus X, Barraza N, Calco V, Houy S, Couve E, Neely A, Martínez AD, Gasman S, Cárdenas AM (2013) Dynamin-2 regulates fusion pore expansion and quantal release through a mechanism that involves actin dynamics in neuroendocrine chromaffin cells. PLoS One. 8:e70638.
  • Cárdenas AM, Marengo FD (2016) How the stimulus defines the dynamics of vesicle pool recruitment, fusion mode, and vesicle recycling in neuroendocrine cells. J Neurochem. 137:867-79.
  • Cárdenas AM, González-Jamett AM, Cea LA, Bevilacqua JA, Caviedes P (2016) Dysferlin function in skeletal muscle: Possible pathological mechanisms and therapeutical targets in dysferlinopathies. Exp Neurol. 283:246-54.
  • González-Jamett AM, Baez-Matus X, Olivares MJ, Hinostroza F, Guerra-Fernández MJ, Vasquez-Navarrete J, Bui MT, Guicheney P, Romero NB, Bevilacqua JA, Bitoun M, Caviedes P, Cárdenas AM (2017) Dynamin-2 mutations linked to Centronuclear Myopathy impair actin-dependent trafficking in muscle cells. Sci Rep. 7:4580.
  • Vásquez-Navarrete J, Martínez AD, Ory S, Baéz-Matus X, González-Jamett AM, Brauchi S, Caviedes P, Cárdenas AM (2018) RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome. Front Cell Neurosci. 12:189.
  • García-Campos P, Báez-Matus X, Jara-Gutiérrez C, Paz-Araos M, Astorga C, Cea LA, Rodríguez V, Bevilacqua JA, Caviedes P, Cárdenas AM (2020) N-Acetylcysteine Reduces Skeletal Muscles Oxidative Stress and Improves Grip Strength in Dysferlin-Deficient Bla/J Mice. Int J Mol Sci. 21:4293.
  • Maldifassi MC, Momboisse F, Guerra MJ, Vielma AH, Maripillán J, Báez-Matus X, Flores-Muñoz C, Cádiz B, Schmachtenberg O, Martínez AD, Cárdenas AM (2020) The interplay between α7 nicotinic acetylcholine receptors, pannexin-1 channels and P2X7 receptors elicit exocytosis in chromaffin cells. J. Neurochem. doi: 10.1111/jnc.15186.


  • 2012- : With P. Caviedes and Jorge Bevilacqua  (I.C.B.M., Facultad de Medicina, Universidad de Chile): Molecular and cellular mechanisms of muscular dystrophy related to mutations of dysferlin. Proyecto Anillo ACT1121.
  • 2016- : With Dr. Fernando Marengo (Universidad de Buenos Aires).
  • 1995- : With Dr. P. Caviedes (I.C.B.M., Facultad de Medicina, Universidad de Chile): Intracellular calcium homeostasis in neuronal cell lines derived from trisomy 16 mouse, a model of human trisomy 21 (Dow Syndrome) Granted by DIPUV 2896 y 0398 and Fondecyt 1980906, 1040862, 1090160.
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