- Terza Missione
- Il BO Live
2001-present: Research Scientist, Neuroscience Institute, National Research Council (CNR), Padua.
2000-2001: Telethon fellow, Dept. of Biomedical Sciences, University of Padua.
1998-2000: Postdoctoral Fellow, Dept. of Experimental and Molecular Cardiology, Academic Medical Center, Amsterdam, The Netherlands.
1995–1998: Postdoctoral Fellow, Institute for Genetics, Karlsruhe, Germany.
1995: PhD degree in Molecular and Cellular Biology and Pathology, University of Padua.
Dr. Campione studies the molecular basis driving cardiac development and the impact of developmental processes on the functional properties of the adult heart. Ongoing research activity:
1)Understanding cardiac laterality: the role of the homeobox gene Pitx2.
A central challenge in cardiac developmental biology is to understand the mechanisms that regulate the regulate the growth and remodeling of the heart. The homeobox gene Pitx2 is a key regulator of left-right identity in the developing heart and drives cardiac asymmetric development. We are presently dissecting the regional and temporal contribution of the gene to this process by employing both constitutive and myocardial specific Pitx2 knock out mice.
Reduced dosage of the Pitx2 gene has been shown to increase susceptibility to atrial fibrillation in humans and in mice, thus linking laterality to adult heart function. We are additionally exploiting Pitx2 mutant mice to dissect the regional contributions of Pitx2 to arrhythmogenesis.
2)The role of mechanosensing genes in cardiac development and in modulation of adult heart functionality.
Cardiomyocytes, the functional units of the heart, can sense and transduce environmental cues such as mechanical stress and hemodynamics. The mechanosensor protein Ankrd1 is expressed non homogeneously in the embryonic myocardium, with a dynamic nucleo-sarcomeric localization in developing cardiomyocytes. In humans, increased ANKRD1 levels linked to gain of function mutations have been associated to total anomalous pulmonary venous return and adult cardiomyopathy occurrence. By employing a gain of function ANKRD1 mouse we have recently shown that ANKRD1 is a fine mediator of cardiomyocyte response to hemodynamic load in the developing and adult heart. We have shown that increased ANKRD1 levels are sufficient to initiate an altered cellular phenotype, which is progressively exacerbated into a pathological organ response by the high ventricular workload during postnatal life.
1- Piroddi N, Pesce P, Scellini B, Manzini S, Ganzetti GS, Badi I, Menegollo M, Cora V, Tiso S, Cinquetti R, Monti L, Chiesa G, Bleyl SB, Busnelli M, Dellera F, Bruno D, Caicci F, Grimaldi A, Taramelli R, Manni L, Sacerdoti D, Tesi C, Poggesi C, Ausoni S, Acquati F, Campione M. Myocardial overexpression of ANKRD1 causes sinus venosus defects and progressive diastolic dysfunction. Cardiovasc Res. 2020;116(8):1458-1472.
2- Furlan S, Campione M, Murgia M, Mosole S, Argenton F, Volpe P, Nori A. Calsequestrins New Calcium Store Markers of Adult Zebrafish Cerebellum and Optic Tectum. Front Neuroanat. 2020 Apr 21;14:15.
3-Scardigli M, Müllenbroich C, Margoni E, Cannazzaro S, Crocini C, Ferrantini C, Coppini R, Yan P, Loew LM, Campione M, Bocchi L, Giulietti D, Cerbai E, Poggesi C, Bub G, Pavone FS, Sacconi L. Real-time optical manipulation of cardiac conduction in intact hearts. J Physiol. 2018 Sep;596(17):3841-3858.
4-Ulmer B, Tingler M, Kurz S, Maerker M, Andre P, Mönch D, Campione M, Deißler K, Lewandoski M, Thumberger T, Schweickert A, Fainsod A, Steinbeißer H, Blum M. (2017). A novel role of the organizer gene Goosecoid as an inhibitor of Wnt/PCP-mediated convergent extension in Xenopus and mouse. Sci Rep.;7:43010.
5-Campione M and Franco D. Current Perspectives in Cardiac Laterality (2016). J. Cardiovasc. Dev. Dis. 2016, 3(4), 34.
6-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.