G. Ian Gallicano, PhD

G. Ian Gallicano, PhD

Associate Professor
Department of Cell Biology
Georgetown University Medical Center
NE203 Med-Dent Building, Box 571436
3900 Reservoir Road, NW
Washington, DC 20007 
Phone: 202 687-0228
Fax: 202 687-1823

Research Interests

Embryogenesis, Tumorigenesis, Embryonic Stem Cell Research

Research Summary 

I focus on cellular adhesion in capillary formation during early embryogenesis in mammals, and then uses this knowledge to investigate capillary formation in tumors of different sexes (e.g., breast cancer vs. prostate cancer) so as to block tumor vascularization.

Currently, two projects are ongoing in my laboratory. The first project investigates cellular adhesion in capillary formation during early embryogenesis in mammals. We then apply that knowledge to capillary formation in tumors so as to block tumor vascularization. To do so, we use three distinct biological disciplines, Microscopic, Molecular, and Biochemical analyses, all of which have begun to shed light on the importance of certain components involved with cellular adhesion during capillary formation in the embryo. One specific cell adhesion component we work on is desmoplakin, a major building block of junctions known as complexus adherens junctions in cells that comprise capillaries. To study desmoplakin in detail we have used embryonic stem cell technology to “knock out” the desmoplakin gene in mice. Embryos that lack desmoplakin die about 6 days after fertilization because they fail to expand their egg cylinders (the main structure that houses the embryo in the uterus). Partial rescue of these embryos using a technique called tetraploid aggregation revealed that capillaries lacking desmoplakin fail to form properly causing embryonic lethality at embryonic Day 10. Numerous other problems (e.g., decreased cellular proliferation) also are found in these early stage embryos lacking desmoplakin and we are currently trying to determine how the loss of desmoplakin causes these problems during development.

The second project in the laboratory investigates a mutant form of desmoplakin (DP) that causes distinct cardiomyopathies (left ventricular dilated forms), which was recently discovered in children (Norgett et al., 2000). This finding begs further investigation using in-vitro cell culture and mice as model systems for understanding, in more detail, the onset of the disease pathology and possible ways to correct it. To date, however, except for our laboratory, few models have been produced with mutations in DP resulting in heart defects.

Representative Publications

  • Zhou, X., Quann, E., Gallicano, G.I., (2003) Differentiation of non-beating embryonic stem cells into beating cardiomyocytes is dependent upon down regulation of PKCß and z in concert with up regulation of PKCe Developmental Biology 255:407-422.
  • Gallicano, G.I., (2001). Composition, regulation, and function of the cytoskeleton in mammalian eggs and embryos. Frontiers in Bioscience (6:d1089-1108).
  • Gallicano, G.I., Bauer, C., and Fuchs E. (2001) Rescuing Desmoplakin Function in extraembryonic ectoderm reveals an importance for desmoplakin in embryonic heart, neurepithelium, skin, and vasculature. Development, 128(6) 929-941.
  • Gallicano, G.I., P. Kouklis, C. Bauer, M. Yin, V. Vasioukin, L Degenstein, and E. Fuchs. (1998). Desmoplakin is required early in development for assembly of desmosomes and cytoskeletal linkage. Journal of Cell Biology 143:2009-2022. COVER PHOTOGRAPH
  • Gallicano, G.I., R.W. McGaughey, and D.G. Capco. (1997). Activation of protein kinase C after fertilization is required for remodeling the mouse egg into the zygote. Molecular Reproduction and Development. 46:587-601.