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Neonatology

Thomas Bartman

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Thomas Bartman, MD, PhD

Appointment

Assistant Professor of Pediatrics

Email

thomas.bartman@cchmc.org

Phone

513-636-9902

Fax

513-636-7868

Bio

Approximately 1% of newborns have structural malformations of the heart, making congenital heart disease (CHD) a leading cause of neonatal morbidity and mortality. While some infants with CHD have defined genetic syndromes, such as DiGeorge syndrome or Holt-Oram syndrome, the majority of cases are non-syndromic. Because the risk of CHD in siblings of patients with CHD is increased 2-3 fold above the population risk, there is clearly a genetic component to the development of CHD even in the absence of a clearly defined syndrome. However, very little is known about the genetics of CHD and have identified very few genes as being predisposing to or causative of CHD.

Thomas Bartman, MD, PhD's, lab uses the zebrafish to attempt to identify genes which are critical for the proper morphogenesis of the heart. The zebrafish is ideal for such studies because the embryos are externally fertilized and transparent, which allows for the direct visualization of the heart during organogenesis, and because of the ability to do forward-genetic studies in the zebrafish. The later feature allows for random introduction of mutations into the genome to assay for developmental perturbations that result from the introduced mutations. In this way, all of the genes involved in a developmental process can be identified in an un-biased fashion.

Dr. Bartman's previous work has focused on the zebrafish line cardiofunk, in which endocardial cushions do not form. cfk encodes a novel actin expressed in the heart during organogenesis, and the cfks11 allele contains a dominant negative mutation which interferes with myocardial function. This led to the discovery that myocardial function is required for the development of endocardial cushions, as verified in studies with silent heart embryos and embryos treated with inhibitors of myofibrillar ATPase. What has not been answered is the exact mechanism by which contractility affects cushion development. One possibility is that alterations in blood flow affect shear stresses on the endocardial cells, which is well known to be important in affecting the gene expression profiles of endocardial cells. Another possibility is that altered myocardial function affects the expression or secretion of molecules that are required to signal to the endocardium to initiate cushion development. One focus of the Bartman lab will be to address this very issue.

The lab will have two other veins of research. First is to positionally clone other mutants identified with defects in endocardial cushion development. Second, the screens that have been performed to look for cushion development have been neither particularly sensitive nor specific. The lab will perform another forward genetic screen in transgenic fish to allow for the better visualization of cushion/valve morphology and to identify more genes involved in cushion/valve morphogenesis.

Credentials

Baccalaureate: Massachusetts Institute of Technology, Life Sciences, 1989
MD/PhD: Molecular Biology and Genetics, Temple University, Philadelphia, PA, 1996.
Residency: Pediatrics, University of California, San Francisco, 1996-1999.
Fellowship: Neonatology, University of California, San Francisco, 1999-2003.
Postdoctoral Research: Cardiovascular Research Institute (Didier Stainier), UCSF, 2000-2003.
Certification: Pediatrics, 1999. Neonatology, 2003.

Position History

Assistant Professor, Divisions of Developmental Biology, Pulmonary Biology and Neonatology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 2003 - present

Awards and Honors

  • Melvin Grumbach Award for Postdoctoral Research, UCSF Department of Pediatrics, 2003
  • Weinstein Cardiovascular Development Conference, Outstanding Presentation, 2002
  • Mary DeLeo Award for Outstanding Research in Oncology, Temple University, 1996

Research

Cardiovascular development in zebrafish, especially endocardial cushion and heart valve development.

Congenital heart disease in newborns; genetic factors influencing heart malformations in the fetus and newborn.

Visit the Bartman Lab web site.

Research Grants and Contracts

Howard Hughes Medical Institute 9/2000-7/2003, Postdoctoral Research Fellowship for Physicians.

NIH K12HD28827 9/2003-8/2005

American Heart Association Scientist Development Grant 1/2006-12/2009, Analysis of NFATc1 as the Mechanism by which Early Heart Function Regulates Endocardial Cushion and Valve Morphogenesis

March of Dimes 6/2006-5/2009, Role of Chondroitin and Dermatan Sulfatation in Endocardial Cushion Morphogenesis

Publications, Most Recent

Thomas Bartman's publications as listed by PubMed

Professional Organization Memberships

  • Society for Pediatric Research

Invited Research Presentations


Bartman, T.; Walsh, E.; Wen, K.; McKane, M.; Ren, J.; Alexander, J.; Rubenstein, P.A.; Stainier, D.Y.R.: Altered Cardiac Contractility Disrupts Proper Cushion Morphogenesis. Weinstein Cardiovascular Development Conference, May 15-17, 2003; Boston, MA.

Bartman, T.; Walsh, E.; Stainier, D.Y.R.: A Mutation in a Novel Actin Disrupts Endocardial Cushion Formation in Zebrafish. Weinstein Cardiovascular Development Conference, May 16-18, 2002; Salt Lake City, UT.

Related Areas

This person works in these other areas at Cincinnati Children's Hospital Medical Center: