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Andy Wessels Ph.D.

Arno Wessels Ph.D.

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Rank
  • Professor
College
  • College of Medicine
Department
  • Regenerative Medicine and Cell Biology
Academic Focus
  • Mechanisms of Heart Development
  • Pathogenesis of Congenital Heart Disease
  • Etiology of Valve Disease
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Biography

Dr. Andy (Arno) Wessels was born and raised in The Netherlands. In 1991 he received his PhD from the University of Amsterdam for his studies on the development of the human heart. Between 1991 and 1994 he continued these studies as a postdoctoral fellow/visiting scientist at the University of Amsterdam and at the National Heart and Lung Institute in London, UK. In 1994 he accepted an offer to join the Department of Cell Biology and Anatomy at MUSC as a Visiting Research Assistant. He subsequently joined the faculty as an assistant professor in 1996, was promoted to associated professor in 2001, and to full professor with tenure in 2010. In 2015 he became the vice-chair of the Department of Regenerative Medicine and Cell Biology (formerly known as the Department of Anatomy and Cell Biology).

 

 Research Program : Each year, nearly twice as many children die in the United States from congenital heart disease (CHD) as from all forms of childhood cancers combined. In the western world, the incidence of CHD varies from 8-10/1000 in the live newborn population. The overall goal of the research performed in the Wessels Laboratory is to unravel the developmental events that are involved in normal cardiac development and to elucidate the mechanisms that lead to congenital heart malformations.  In addition, research in the lab also aims at elucidating developmental mechanisms that may be involved in the pathogenesis of so-called acquired heart diseases. The lab currently focusses on two major research projects:

 

1. Elucidating the Role of the Dorsal Mesenchymal Protrusion (DMP) in the Pathogenesis of Atrioventricular Septal Defects (AVSD): Atrioventricular septal defects (AVSDs) form a class of congenital heart malformations found in approximately 5% of all persons suffering from congenital heart disease (CHD). AVSDs are particularly prevalent in the spectrum of defects associated with genetic disorders such as Heterotaxy Syndrome and Down Syndrome. In recent years, the understanding of the molecular etiology and morphological mechanisms associated with the pathogenesis of AVSDs has significantly changed. Specifically, studies from our lab have linked abnormal development of the Dorsal Mesenchymal Protrusion (DMP), a Second Heart Field-derived structure, to the pathogenesis of this congenital defect (Snarr et al., 2007a, Snarr et al., 2007b; Briggs et al., 2012, 2013, 2016). In ongoing research in the lab we aim a) to elucidate how molecular pathways that drive normal DMP development interact (including the Shh, Bmp and Wnt/beta catenin pathways), b) to determine the DMP-associated cellular mechanisms that result in AVSDs, and c) to develop strategies that ultimately will decrease the incidence of AVSDs in the human population.



2. Establishing the Role of Epicardially-derived Cells (EPDCs) in Valvuloseptal Development: The atrioventricular (AV) valves serve to assist in unidirectional blood flow through the heart. For many years, it was believed that the cells that populate the valves during development were all endocardially-derived. However, in studies from the Wessels lab it was determined that the epicardium, an epithelial cell layer on the surface of the heart, significantly contributes to a subset of the leaflets of the AV valves as well. In fact, the epicardially-derived cells (EPDCs) specifically contribute to the parietal AV valve leaflets, whereas the AV valve leaflets that are associated with the ventricular septum do not contain significant numbers of EPDCs (Wessels et al., 2012). That the EPDCs are important for valve formation was demonstrated in additional studies in which we manipulated Bmp signaling in the epicardial cell lineage. This experimental approach resulted in a reduction of the number of EPDCs in the leaflets and eventually a myxomatous valve phenotype reminiscent of that seen in patients that suffer from valve disease (Lockhart et al., 2014a; Lockhart et al., 2014b). We are currently investigating how the preferential migration of EPDCs into the parietal leaflets is regulated and what the role of EPDCs is in relation to congenital and acquired defects of the AV valves.