Robert M. Lavker, PhD
Professor of Dermatology
Director, Dermatology Research
Email: r-lavker@northwestern.edu
Biography
Dr. Robert Lavker is currently Professor of Dermatology at Northwestern and Director of Dermatology Research. He completed his undergraduate training at the University of Delaware and his PhD. Training at Clemson University. He also received an honorary Master’s degree from the University of Pennsylvania. His performed postdoctoral fellowship training at the Boston University School of Medicine, where he subsequently served as an Assistant Professor.
After another fellowship year at the University of Pennsylvania, he joined the faculty at University of Pennsylvania where he was promoted to Professor and served as Director of Research for their Department of Dermatology. He joined the research faculty in the Department of Dermatology at Northwestern in 2002 as the Director of Research.
Dr. Lavker has served on the Board of Directors of the Society for Investigative Dermatology, and is currently an Associate Editor of the Journal of Investigative Dermatology. He is the author of approximately 150 papers, reviews and chapters related to dermatological research. He is particularly interested in hair biology, stem cells and photoaging.
Research Interests
Dr. Lavker's laboratory has centered on investigations of processes of proliferation and differentiation in keratinizing tissues. In collaboration with Tung-Tien Sun, my laboratory has been engaged in continued studies on the biology of epithelial stem cells. To this end we have identified and characterized a novel protein EEDA (early epithelial differentiation-assocated protein) that is, as its name implies, associated with an early stage of stratified epithelial differentiation. We have also cloned and sequenced the promoter for this gene and studies are ongoing to understand better how this gene is regulated. A mutant mouse deficient in EEDA is being generated in an attempt to learn more about the function of this protein. In conjunction with the Wolosin laboraory (Mt. Sinai), we localized an ABCG2-dependent side population (SP) of cells in the limbal and conjunctival epithelia that exhibited features consistent with stem cells. The SP cells were characterized by extremely low light side scattering and contained a high percentage of cells that: showed slow-cycling prior to tissue collection; exhibited an initial delay in proliferation after culturing; and displayed clonogenic capacity and resistance to phorbol-induced differentiation; all features that are consistent with a stem cell phenotype. We are planning to transcriptionally profile these SP cells in hopes of finding some stem cell-enriched surface markers.
More recently, my laboratory has successfully employed laser capture microdissection to isolate pure populations of limbal epithelial basal cells (enriched in stem cells) and corneal epithelial basal cells (enriched in stem cell progeny). Analysis of RNA isolated from these cell populations revealed a set of ~100 genes that were differentially expressed in the limbal basal cells versus the corneal basal cells. Semi-quatitative RT-PCR confirmed the up-regulation of 3 limbal and 3 corneal genes. LacZ identification of epiregulin from epiregulin-null mice and immunohistochemical staining of wild type mice confirmed that epiregulin, one of the limbal epithelium-enriched genes, was associated exclusively with the limbal epithelial basal cells. Within the limbal and corneal basal cells we detected previously unknown genes that were differentially expressed in these two regions that contribute further to our understanding of the unique heterogeneity of these two closely related basal cell populations.
Finally, the laboratory has begun to characterize microRNAs (miRNAs) found in the stem cells of the epidermis and corneal epithelium; and (ii) understand how miRNAs regulate stem cell proliferation and differentiation. MiRNAs are a family of endogenous, small RNAs that regulate the expression of complementary messenger RNAs by acting as post-translational repressors. MiRNAs have been shown to function in development, cell death, cell proliferation, differentiation, and the initiation and progression of cancer. Significantly, a subset of miRNAs has been identified that are expressed in stem cells, but are lost when these cells differentiate. Our preliminary results demonstrate the presence of several miRNAs that are specifically localized in the corneal epithelium of adult mice; other miRNAs are found in many stratified squamous epithelia including the epidermis. Recently we have found that the lipid phosphatase SHIP2 is a target for microRNA- 205 (miR-205), which is expressed in many stratified squamous epithelia. We have also found that miR-184, which is exclusively found in the corneal epithelium, antagonizes miR-205 to help maintain the levels of SHIP2. Finally, we have evidence that miR-205 may be functioning as a tumor promoter in squamous cell carcinomas through the negative regulation of the AKT pathway.