Heart-specific Deletion of CnB1 Reveals Multiple Mechanisms Whereby Calcineurin Regulates Cardiac Growth and Function

Current position: Research associate in the laboratory of Jeffery D. Molkentin at the University of Cincinnati, Cincinnati Children's Hospital

Education: Ph.D. in molecular and cellular biology in 2003 from the Université de Médecine, Paris XI in France

Nonscientific interests: Equestrian riding and snow skiing

I started my research career in Spain during an undergraduate European inter-university exchange program. I was fascinated by hormone/receptor interactions and associated intracellular signaling pathways. After this first research experience, I started my Ph.D. thesis project in 2000 at the University of Medicine of Paris XI (France). This work characterized signaling pathways initiated by serotonin in the cardio-vascular system. After my Ph.D. was awarded in 2003, I decided to orientate my career toward a broader vision of the cardiovascular system. I, thus, joined the laboratory of Dr. Jeffery D. Molkentin at the University of Cincinnati, Children's Hospital. Dr. Molkentin's laboratory uses mouse genetic approaches to characterize signaling pathways that regulate cardiac hypertrophy and heart failure. One of my projects during my postdoctoral training centered on calcineurin/NFAT signaling in the heart, which is a well-known transducer of calcium signaling-induced hypertrophy and disease. Calcineurin is a calcium-activated phosphatase that mediates, through the dephosphorylation of NFAT transcription factors, the transcription of inducible genes involved in the establishment of cardiac hypertrophy. In this publication, we used mouse genetics to turn off essentially all calcineurin activity in the developing and the adult mouse heart. Remarkably, this study uncovered a novel signaling relationship whereby calcineurin appears to directly control gene expression of calcium regulatory proteins in the heart. This relationship seems to profoundly affect myocyte proliferation, growth, cardiac contractility, arrhythmia susceptibility and adaptation to cardiac stress.

Read Maillet's article on page 6716.