Marina Campione
e-mail: campione AT bio.unipd.it
affiliation: National Research Council (CNR)
research area(s): Genetics And Genomics, Developmental Biology
Course:
Biosciences and Biotechnologies
University/Istitution: Università di Padova
University/Istitution: Università di Padova
Degree in Biological Sciences at the University of Padua, Italy (13/3/1987)
Academic qualifications:
17/10/1995: Ph.D degree on Molecular and Cellular Biology and Pathology (University of Padua, Italy). Ph.D thesis title: Analysis of the structure and regulation of cardiac troponin I gene promoter.
Current position:
Scientist at the National Research Council-Institute of Neurosciences (Dept.of Biomedical Sciences, University of Padua, Italy).
Principal Investigator of the Genetics of cardiovascular development group.
Research interests: genetic basis of cardiac development and disease, with a focus on laterality genes.
Former positions:
10/2000-12/2001: Telethon scientist at the Dept. of Biomedical Sciences, University of Padua, Italy.
6/1999-9/2000: Post-doc in the lab. of Prof. Antoon Moorman (Dept. of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, The Netherlands).
3/1995-5/1999: Post-doc in the lab. of Dr. Martin Blum (Institute for Genetics, Karlsruhe Research Center, Germany).
1991-1995: Ph.D. student in the lab. of Prof. S. Schiaffino (Department of Biomedical Sciences, University of Padua, Italy).
1989-1990: Research fellow in the the lab.of Prof. Schiaffino (Dept.of Biomedical Sciences, University of Padua, Italy).
1987-1989: Research fellow of the Glaxo Industry (Verona, Italy).
Academic qualifications:
17/10/1995: Ph.D degree on Molecular and Cellular Biology and Pathology (University of Padua, Italy). Ph.D thesis title: Analysis of the structure and regulation of cardiac troponin I gene promoter.
Current position:
Scientist at the National Research Council-Institute of Neurosciences (Dept.of Biomedical Sciences, University of Padua, Italy).
Principal Investigator of the Genetics of cardiovascular development group.
Research interests: genetic basis of cardiac development and disease, with a focus on laterality genes.
Former positions:
10/2000-12/2001: Telethon scientist at the Dept. of Biomedical Sciences, University of Padua, Italy.
6/1999-9/2000: Post-doc in the lab. of Prof. Antoon Moorman (Dept. of Anatomy and Embryology, Academic Medical Center, University of Amsterdam, The Netherlands).
3/1995-5/1999: Post-doc in the lab. of Dr. Martin Blum (Institute for Genetics, Karlsruhe Research Center, Germany).
1991-1995: Ph.D. student in the lab. of Prof. S. Schiaffino (Department of Biomedical Sciences, University of Padua, Italy).
1989-1990: Research fellow in the the lab.of Prof. Schiaffino (Dept.of Biomedical Sciences, University of Padua, Italy).
1987-1989: Research fellow of the Glaxo Industry (Verona, Italy).
The heart is the first organ to form and function in the embryo and its structural and functional integrity are crucial for the quality of adult life. Understanding the molecular pathways that regulate cardiac growth and function is crucial to prevent and cure heart disease.
The homeobox gene Pitx2 is a crucial player both in cardiac development and for prevention of adult functional disease. Pitx2 regulates left atrial morphological and molecular identity and asymmetric ventricular remodelling in the developing heart; the crucial role of the gene is outlined by the complex cardiac phenotype of constitutive and myocardial specific ko of the gene. Moreover, Pitx2 has been indicated as a susceptibility gene for atrial arrhythmias. SNP close to the PITX2 locus correlate with atrial fibrillation (AF) onset in humans, and reduced gene dosage leads to arrhythmia susceptibility in humans and mice. The link between SNPs, Pitx2 expression, onset and perpetuation of AF and arrhythmia is not jet clear.
Research in our laboratory is aiming 1) to dissect the molecular bases for Pitx2 action in the developing heart; 2) to analyze the molecular and functional mechanisms underlying genetic susceptibility to atrial fibrillation as a consequence of reduced Pitx2 dosage. We employ molecular and cellular biology approaches as well as in vivo physiological analysis on conditional ko mouse models.
The homeobox gene Pitx2 is a crucial player both in cardiac development and for prevention of adult functional disease. Pitx2 regulates left atrial morphological and molecular identity and asymmetric ventricular remodelling in the developing heart; the crucial role of the gene is outlined by the complex cardiac phenotype of constitutive and myocardial specific ko of the gene. Moreover, Pitx2 has been indicated as a susceptibility gene for atrial arrhythmias. SNP close to the PITX2 locus correlate with atrial fibrillation (AF) onset in humans, and reduced gene dosage leads to arrhythmia susceptibility in humans and mice. The link between SNPs, Pitx2 expression, onset and perpetuation of AF and arrhythmia is not jet clear.
Research in our laboratory is aiming 1) to dissect the molecular bases for Pitx2 action in the developing heart; 2) to analyze the molecular and functional mechanisms underlying genetic susceptibility to atrial fibrillation as a consequence of reduced Pitx2 dosage. We employ molecular and cellular biology approaches as well as in vivo physiological analysis on conditional ko mouse models.
Ammirabile G, Tessari A, Pignataro V, Szumska D, Sardo FS, Benes J Jr, Balistreri M, Bhattacharya S, Sedmera D, Campione M.(2012). Pitx2 confers left morphological, molecular, and functional identity to the sinus venosus myocardium. Cardiovasc Res. 93,291-230.
Tessari A, Pietrobon M, Notte A, Cifelli G, Gage PJ , Schneider MD, Lembo G, Campione M.(2008). Myocardial Pitx2 differentially regulates the left atrial identity and ventricular asymmetric remodelling programs. Circ. Res 102,813-822.
Cinguetti R, Badi I, Campione M, Bortolotto E, Chiesa G, Parolini C, Camesasca C, Russo A, Taramelli R, Acquati F (2008). Transcriptional deregulation and a missense mutation define ANKRD1 as a candidate gene for Total Anomalous Pulmonary Venous Return. Human Mutation 29, 468-74.
Aggarwal VS, Liao J, Bondarev A, Schimmang T, Lewandoski M, Locker J, Shanske A, Campione M, Morrow BE (2006). Dissection of Tbx1 and Fgf interactions in mouse models of 22q11DS suggests functional redundancy. Hum Mol Genet. 15, 3219-28.
Campione M, Franco D, Kelly R (2006). Cardiovascular development: towards biomedical applicability. Dev Dyn 235, 843-5.
Nowotschin S, Liao J, Gage PJ, Epstein JA, Campione M, Morrow BE (2006). Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field. Development. 133,1565-73
Tessari A, Pietrobon M, Notte A, Cifelli G, Gage PJ , Schneider MD, Lembo G, Campione M.(2008). Myocardial Pitx2 differentially regulates the left atrial identity and ventricular asymmetric remodelling programs. Circ. Res 102,813-822.
Cinguetti R, Badi I, Campione M, Bortolotto E, Chiesa G, Parolini C, Camesasca C, Russo A, Taramelli R, Acquati F (2008). Transcriptional deregulation and a missense mutation define ANKRD1 as a candidate gene for Total Anomalous Pulmonary Venous Return. Human Mutation 29, 468-74.
Aggarwal VS, Liao J, Bondarev A, Schimmang T, Lewandoski M, Locker J, Shanske A, Campione M, Morrow BE (2006). Dissection of Tbx1 and Fgf interactions in mouse models of 22q11DS suggests functional redundancy. Hum Mol Genet. 15, 3219-28.
Campione M, Franco D, Kelly R (2006). Cardiovascular development: towards biomedical applicability. Dev Dyn 235, 843-5.
Nowotschin S, Liao J, Gage PJ, Epstein JA, Campione M, Morrow BE (2006). Tbx1 affects asymmetric cardiac morphogenesis by regulating Pitx2 in the secondary heart field. Development. 133,1565-73
No projects are available to students for the current accademic year.