Heather Szabo Rogers BSc PhD

Assistant Professor
Dr. Heather Szabo Rogers is an Assistant Professor in Oral Biology in the School of Dental Medicine at the University of Pittsburgh with a secondary appointment in the Department of Developmental Biology and the McGowan Institute of Regenerative Medicine. Dr. Rogers is the Vice President of the Pittsburgh chapter of AADR.
 
Dr. Rogers graduated with a B.Sc. in Cell Biology from the University of Alberta in Edmonton Canada, and completed her PhD at the University of British Columbia. Dr. Rogers completed a postdoc at King’s College London and joined the faculty of the University of Pittsburgh in 2012.
 
Dr. Rogers research interests focus on the development of the craniofacial complex – the skull, cranial base, lip and palate and can be broadly focused into three arms. 1) Developmental etiology including molecular and cellular  mechanisms in the development of orofacial clefting. 2) Control and development of the skull vault and cranial base. 3) Cell polarization and orientation functions in craniofacial development. To address these questions, using a combination of classical embryology and cell biological techniques. Our work will help us understand how craniofacial anomalies including cleft lip and palate and craniosynostosis arise during embryogenesis.
 
Dr. Rogers has both refereed primary research articles and review articles. She is a member of: Society for Craniofacial Genetics, Society of Developmental Biology, British Society of Developmental Biology, International Association of Dental Research, American Association of Dental Research and Canadian Association of Dental Research. Dr. Rogers reviews manuscripts for the Journal of Anatomy, Cleft Palate Craniofacial Journal, Developmental Dynamics, and the Journal of Dental Research amongst others. 
Education & Training
University of Alberta, BS 2000
University of British Columbia, PhD 2007
Research Interests

Dr. Rogers’ research focuses on development of the craniofacial complex, -- chiefly the skull, cranial base, lip and palate -- and seeks to discover how craniofacial anomalies including cleft lip and palate and craniosynostosis arise during embryogenesis . Her work addresses these questions through a combination of classical embryology and cell biological techniques and encompasses the following areas:

Developmental etiology including molecular and cellular mechanisms in the development of orofacial clefting

Using mouse models, Dr. Rogers and colleagues are working to understand development of cleft lip and palate. Dr. Rogers hypothesizes that in the developing face, an appropriate merging of skeletogenic condensations must occur in the frontonasal process and cranial base. In several mouse models, Dr. Rogers and her research team have observed defects in midline merging. They are working to determine the genetic and mechanistic defects underlying these defects – testing whether they arise from increased proliferation, decreased cell death and/or from changes in signaling that prevent condensations from merging. Dr. Rogers’ expects the data to identify novel mechanisms and genes that contribute to orofacial clefting.

Control and development of the skull vault and cranial base

Skull vault and cranial base mineralization and maturation are intriguing because of the former’s process of intramembraneous ossification and the latter’s endochondral ossification. Both of these structures are of composite cell origin, with the more anterior regions being derived from the neural crest and the more posterior being developed from mesoderm.

Dr. Rogers and colleagues have observed significant defects in the heads of Beetlejuice mutants, which have a missense mutation in Prickle1Prickle1 is a core component of the Wnt/planar cell polarity pathway.  The Wnt/PCP pathway polarizes cytoplasmic constituents and enables for asymmetric secretion and division. An open question in the field is how these processes contribute to normal and abnormal craniofacial development and, in particular, how the development of the neural crest-derived regions of the skull use this pathway in at least two phases of migration. Dr. Rogers’ lab is currently working to determine whether defective migration and/or differentiation cause the phenotypes seen in the Beetlejuice mutants.

Cell polarization and orientation functions in craniofacial development  

Dr. Rogers and her team have recently shown that Dspp-/-enamel undergoes accelerated differentiation. Dsppis translated and transcribed as a pre-protein. Post-translation modification involves cleavage into two proteins—dentin phosphoprotein (Dpp) and dentin sialophosphoprotein (DSP). The Dspp-/-mice lack both of these proteins. In preliminary analysis, Dr. Rogers’ and her team have found that the odontoblast and osteoblasts have developmental effects. Current work in this area focuses on testing to determine if these defects arise from defects in polarization and orientation.

Administrative

Michele Leahy
412-648-3903
mmp2@pitt.edu