Heart Chamber Development
Valvuloseptal Development and Congenital Heart Disease Mechanisms
Defects in heart chamber and valve development represent the largest classes of human congenital cardiac anomalies and can be caused by environmental factors or genetic mutations. Studies are in progress to identify molecular regulatory pathways that control normal and abnormal heart formation. We are examining the signaling pathways and transcription factors that control cardiac valve lineage development, extracellular matrix remodeling and chamber septation in chicken and mouse embryos.
Related Publications
Yutzey, K.E. and Benson, D.W. (2003) TBX5: a developmental key that fits many locks. Invited editorial J. Mol. Cell Cardiol. 35:1175-1177.
Lange A.W., J.D. Molkentin, and K.E. Yutzey. (2004) DSCR1 gene expression is dependent on NFATc1 during cardiac valve formation and colocalizes with anomalous organ development in trisomy 16 mice. Dev. Biol. 266:346-360.
Liberatore CM and K.E. Yutzey (2004). Calcineurin signaling in avian cardiovascular development. Dev. Dynam. 229:300-311.
Lincoln, J., C.M. Alfieri and K.E. Yutzey (2004) Development of heart valve leaflets and supporting apparatus in chicken and mouse embryos. Dev Dynam. 230: 239-250 (cover article).
Plageman, T.F. Jr. and K.E. Yutzey (2004) Differential expression and function of Tbx5 and Tbx20 in cardiac development. J. Biol. Chem. 279: 19026-19034.
Liberatore CM and KE Yutzey (2004). MAP Kinase signaling in avian cardiovascular development. Dev. Dynam. 230:773-780.
Plageman TF Jr. and KE Yutzey (2005). T-box genes and heart development: Putting the "T" in HearT. Dev. Dynam. 232:11-20.
Hinton RB Jr., KE Yutzey, and DW Benson (2005). Congenital heart disease: Genetic causes and developmental insights. Progress in Pediatric Cardiology 20:101-111.
Lange AW BA Rothermel, and KE Yutzey (2005). Restoration of DSCR1 to disomy in Trisomy 16 mice does not prevent Down syndrome-related cardiac or craniofacial development anomalies. Dev. Dynam. 233:954-963.
Krenz M KE Yutzey J Robbins (2005). The Noonan syndrome mutation Q79R in Shp2 increases proliferation of valve primordia mesenchymal cells via ERK1/2 signaling. Circ. Res. 97:813-820.
Yutzey KE, MC Colbert, J Robbins (2005). Ras-related signaling pathways in valve development: Ebb and flow. Physiol. 20:390-397.
Clark KL, KE Yutzey, DW Benson (2006). Transcription factors and congenital heart defects. Ann. Rev. Physiol. 68:91-121.
Lincoln J, CM Alfieri, KE Yutzey (2006). BMP and FGF regulatory pathways control cell lineage diversification of heart valve precursor cells. Dev. Biol. In press.
Lange AW and KE Yutzey (2006). NFATc1 expression in the developing heart valves is responsive to the RANKL pathway and is required for endocardial expression of cathepsin K. Dev. Biol. In press.
Contact Katherine Yutzey
Katherine Yutzey, PhD
Division of Molecular Cardiovascular Biology
Cincinnati Children's Hosptial Medical Center
ML7020
3333 Burnet Avenue
Cincinnati, OH 45229
Phone 513-636-8340
Fax 513-636-5958
Email yutzey@cchmc.org
