Edward Gresik, Ph.D.

Medical Professor
Cell Biology and Anatomy

School of Biomedical Education

Office: H-310
Phone: (212) 650-6857
Fax: (212) 650-6812
E-mail: ewg@med.cuny.edu

Education

A.B., 1961, Xavier University;
M.S., 1966, Ph.D., 1968, Medical Center, University of Illinois, Chicago.

Research Interests

The principal goal of my research has been to study developmental and hormonal regulation of gene expression, using the mouse submandibular gland as a model system to investigate these phenomena in fetal, prepubescent, mature, and sensecent animals. The current focus of my work is the fetal mouse submandibular gland, examined both in vivo and in vitro. During the last third of fetal life, the rudiment of this gland appears, undergoes profuse branching (branching morphogenesis), and differentiates into a variety of distinct cell types. The fact that the fetal gland grown under defined conditions in vitro can replicate all of these developmental events provides an ideal system to study epithelio-mesenchymal interactions that are important for normal development. Several growth factors, notably epidermal growth factor (EGF) and transforming growth factor a (TGF-a) influence the development of this gland. Recent work suggests that components of the extracellular matrix and their receptors (integrins) play essential roles in mediating epithelio-mesenchymal interactions. My laboratory has established that the components of the EGF system regulate branching morphogenesis of the fetal submandibular gland by controlling expression of specific integrins and/or their extracellular ligands during fetal development. Recently we have been investigating the involvement of intracellular signaling cascades triggered by activation of the EGF receptor (ras/Mek/ERK; PLCg1; PI3K; PKC) in regulating branching morphogenesis of the fetal SMG. We employ cell biological and molecular approaches to probe these questions (immunocytochemistry, Western blotting, immunoprecipitation, in situ hybridization, Northern blotting, RT-PCR, nulcease protection assays). The results of these studies will be useful in clarifying mechanisms operating not only in normal fetal development, but also in abnormal events of metastatic spread of malignant growths of epithelial neoplasms (carcinomas), and in identifying strategic points that can be exploited to promote regeneration of damaged salivary tissue.

Publications

Note: Below are the most recent five years of publications for Dr. Gresik. For a more complete list of publications, please go to PubMed at http://www.ncbi.nlm.nih.gov/sites/entrez

PUBLICATIONS IN REFEREED JOURNALS:

• Koyama N, Masanori M, Sakashita H, Sakagami H, Gresik EW. EGF-stimulated signaling via PI3K, PLCg1 and PKC isozymes regulates branching morphogenesis of the fetal mouse submandibular gland. Dev Dyn 227:216-226 (2003).
• Barka T, Gresik EW, Henderson SC. Production of cell lines secreting TAT fusion proteins. J Histochem Cytochem 52:469-477 (2004).
• Kurabuchi S, Gresik EW, Hosoi K. Additive and/or synergistic action (down regulation) of androgens and thyroid hormones on the cellular distribution and localization of a true tissue kallikrein, mK1, in the mouse submandibular gland. J Histochem Cytochem 52:1437-1446 (2004).
• Barka T, Gresik EW, Miyazaki Y. Differentiation of a mouse submandibular gland-derived cell line (SCA) grown on matrigel. Exp Cell Res 308:394-406 (2005).
• Kurabuchi S, Gresik EW, Yao C, Hosoi K. Hypophysectomy and hormonal therapy modulate mK1-immunoreactive duct cells in the mice sublingual glands. J Mol Hist DOI 10.1007/s10735-008-9189-7 (2008)
• Koyama N, Ohno K, Siu L, Gresik EW, Kashimata M. Signaling pathways activated by epidermal growth factor receptor or fibroblast growth factor receptor differentially regulate branching morphogenesis in fetal mouse submandibular glands. Dev Growth Diff 50 (2008) (in press).
  

Last Updated: 9/10/10