- Role: Professore Associato
- Office:U3- II piano stanza 3016
- Telephone number:02- 64483313/3331
- Fisiologia dei Sistemi (Laurea Triennale in Scienze Biologiche, III anno)
- Laboratorio di Fisiologia (Laurea Triennale in Scienze Biologiche, II anno)
The scientific interest concerns different research projects about the cardiac cell physiology; in particular the scientific research is focused on: 1) cardiac diseases, 2) cardiac repolarization anomalies, 3) role and modulation of ion channels, 4) excitation contraction-coupling (EC-coupling), 5) intracellular Ca2+ dynamics, 6) stem cell differentiation.
- Functional genomics, iPS cells, exome sequencing: strategy for the individualized management of arrhythmogenic genetic diseases.
The discovery that somatic cells can be reprogrammed to induced pluripotent stem cells (iPSC) represents an opportunity to generate patient-specific iPSC-derived cadiomyocytes (CM) which recapitulate the cardiac phenotype of the genetic disease. Thanks to a collaboration with P.J. Schwartz group (University of Pavia) we functionally characterized patient-specific iPSC-derived CMs to understand the underlying mechanisms for the most important arrhythmogenic genetic disorders (i.e. the LQT Syndrome). The study is funded by PRIN 2010BWY8E9.
- IP3-R modulation and sarcoplasmic reticulum stability in cellular models of CPVT
Mutations underlying the Catecholaminergic Polymorphic Ventricular Tachycardias (CPVT) syndrome result in sensitization of sarcoplasmic reticulum (SR) Ca2+ channels (RyR2) to intracellular Ca2+, thus facilitating inappropriate Ca2+ release during sympathetic activation. Angiotensin (ATII)-induced activation of SR IP3 receptors (IP3-R) increases Ca2+ near RyR2 channels, which facilitates their opening. While this mechanism may contribute to contractility under normal conditions, its impact on mutant RyR2 channels is currently unknown. Furthermore, ATII increases the synthesis of reactive oxygen species (ROS), further enhancers of RyR2 opening. Thus, the study hypothesize that ATII may facilitate arrhythmogenesis in RyR2 mutants and, therefore, that ATII antagonism may be useful as therapeutic approach to CPVT. The study is funded by PRIN 2010BWY8E9.
- Effects of INaL inhibition in a model of global ischemia.
Reported beneficial effects of the late sodium current (INaL) blockade during global ischemia suggest intracellular Na+ (and Ca2+) overload at the cellular level. To test whether INaL involvement contributes to ischemic damage, isolated cardiac myocytes were exposed to an ischemia-simulating environment. The effect of specific INaL blockers were evaluated on cell shortening, electrical activity and intracellular ions dynamic by video-edge, patch-clamp and epifluorescence techniques respectively. The study is funded by Gilead Sciences (Fremont, CA).