Ruijter J.M.: Cardiac Morphogenesis / Quantitative PCR

The overall aim of my future research is to uncover mechanisms and identify factors that contribute to prenatal development, to postnatal growth and remodelling and to establishment of homeostasis in normal and abnormal cardiac development. During the embryonic and foetal period cardiac structures are formed. Errors in this developmental period result in congenital heart defects. Different cardiac components originate from different populations (fields) of progenitor cells that diverge considerably in their phenotype and sensitivity to developmental defects. After birth, the heart increases in volume and remodels. These processes are influenced by hemodynamic and mechanical forces, although the underlying mechanisms are not known. Furthermore, it is unknown why the regenerative capacity of the heart decreases shortly after birth. Interactions within regulatory networks that control heart development, growth, function and homeostatis will differ in normal and abnormal development, and will be influenced by genetic variation. Current and new methods to quantify gene expression, sequencing and morphogenetic data will serve to study the multivariate associations between morphogenetic,
transcriptional and genomic networks that lead to the different homeostatic states in mouse models with morphological, contraction or conduction defects. My research aims at unravelling the involvement of these networks in cardiac health and disease.