Jane M. Glick
Adjunct Associate Professor, Cell & Developmental Biology

Gene Therapy and Vaccines Program

Address

652 Biomedical Rsch Bldg (BRB) II/III
421Curie Boulevard
Philadelphia, PA 19104-6160

Office tel.: 215-573-7834
Fax: 215-573-8606
E-mail: glickj@mail.med.upenn.edu


Education

Randolph-Macon Woman's College: AB (Chemistry), 1965.

Columbia University: PhD (Biochemistry), 1971.

Research Interests

• atherosclerosis, cellular lipid metabolism.

Search PubMed for articles

Description of Research

Although I no longer have an active laboratory, I continue to be involved in research through collaborations, most closely with Dan Rader. For many years, my research has been focused on cellular lipid metabolism in cells that store lipids - adipocytes, which normally store triglyceride, and “foam cells”, which are hallmarks of an atherosclerotic lesion. The work in adipocytes focused primarily on the role of lipoprotein lipase, a member of the triglyceride lipase family, and its role in providing free fatty acids for storage as triglycerides. The work on foam cells has been much more extensive. In an early atherosclerotic lesion, known as a fatty streak, are cells that have acquired lipid droplets, thus giving the appearance of being filled with foam. The cells types that display this character are largely of macrophage origin in the early lesions, but as the atherosclerotic process progresses, smooth muscle foam cells are also observed. The predominant lipid in foam cells is esterified cholesterol, and work in my laboratory used cell culture models to focus on understanding the mechanisms that 1) govern normal cellular cholesterol homeostasis, 2) allow homeostatic mechanisms to be overcome leading to the deposition of esterified cholesterol, 3) lead to clearance of excess cholesterol from the cells (reverse cholesterol transport), and 4) the role of lipases affecting lipid metabolism in cells and in the plasma compartment. Interest in lipases has been a continuum throughout my research career, which has included work on two members of the triglyceride lipase family, lipoprotein lipase and hepatic lipase, as well as the bile-salt stimulated lipase, hormone-sensitive lipase and lysosomal acid lipase. In recent years, in collaboration with Dan Rader, whose primary interest is prevention of atherosclerosis, I have worked extensively on a new member of the triglyceride lipase family called endothelial lipase. Current work is directed toward reverse cholesterol transport as well as structure/function characterization of endothelial lipase using site-directed mutagenesis and exploration of the physiologic role of endothelial lipase using mouse models.

Recent Publications

Zhang, Y., Zanotti, I., Reilly, M.P., Glick, .JM., Rothblat, G.H., Rader, D.J., Overexpression of apolipoprotein A-I promotes reverse transport of cholesterol from macrophages to feces in vivo. Circulation, 108:661-3, 2003.

Yancey, P.G., Kawashiri, M.A., Moore, R., Glick, J.M., Williams, D.L., Connelly, M.A., Rader, D.J., Rothblat, G.H., In vivo modulation of HDL phospholipid has opposing effects on SR-BI- and ABCA1-mediated cholesterol efflux. J Lipid Res., 45:337-46, 2004.

Broedl, U.C., Maugeais, C., Millar, J.S., Jin, W., Moore, R.E., Fuki, I.V., Marchadier, D., Glick, J.M., Rader, D.J., Endothelial lipase promotes the catabolism of ApoB-containing lipoproteins.
Circ Res. 94:1554-61, 2004.

Miller, G.C., Long, C.J., Bojilova, E.D., Marchadier, D., Badellino, K.O., Blanchard, N., Fuki I.V., Glick, J.M., Rader, D.J., Role of N-linked glycosylation in the secretion and activity of endothelial lipase. J Lipid Res. 45:2080-7, 2004.

Broedl, U.C., Jin, W., Fuki, I.V., Glick, J.M., Rader D.J., Structural basis of endothelial lipase tropism for HDL. FASEB J. 18:1891-3, 2004.

Lab

Rotation Projects for 2006-2007

I do not take students.