Ashrafi, Kaveh
Bernstein, Harold S.
Black, Brian L
Blanc, Paul D
Botvinick, Elias H
Boushey, Homer A
Broaddus, V Courtney
Brodsky, Frances M
Brown, James K
Bruneau, Benoit G
Caughey, George H
Chapman, Harold A
Charo, Israel F
Chatterjee, Kanu
Chuang, Pao-Tien
Clyman, Ronald I
Conklin, Bruce R
Conte, Michael S
Coughlin, Shaun R
Derynck, Rik M
Dobbs, Leland G
Eisner, Mark D
Engel, Joanne N
Erle, David J
Fahy, John Vincent
Farese, Robert V
Fielding, Christopher J
Fineman, Jeffrey R
Gardner, David G
Gartner, Zev Jordan
Glantz, Stanton A
Gold, Warren M
Gropper, Michael
Grossman, William
Hawgood, Samuel
Hill, Arthur C
Hoffman, Julien I
Ingraham, Holly A
Jan, Lily Y
Julius, David J
Kan, Yuet W
Kane, John P
Karliner, Joel S
Kornberg, Thomas B
Kurtz, Theodore W
Kwok, Pui-Yan
Lazarus, Stephen C
Lee, Randall J
Lim, Wendell A
Mahley, Robert W
Malloy, Mary J.
Mann, Michael J
Martin, Gail R
Matthay, Michael A
Mcdonald, Donald M
Mikawa, Takashi
Minor, Daniel L
Mostov, Keith E
Nadel, Jay A
Olgin, Jeffrey E
Pearce, David
Pittet, Jean-Francois
Redberg, Rita F
Reiter, Jeremy F.
Rosen, Steven D
Rowitch, David H
Scheinman, Melvin M
Schiller, Nelson B
Shaw, Robin M.
Sheppard, Dean
Shokat, Kevan M
Simpson, Paul C
Springer, Matthew L
Srivastava, Deepak
Stainier, Didier Y. R.
Teitel, David F
Von Zastrow, Mark E
Wang, Rong
Weiner, Orion D
Weiss, Arthur
Weiss, Ethan J
Werb, Zena
Woodruff, Prescott G
Xu, Allison Wanting
Young, William L

CVRI Scientists

Christopher J Fielding, Ph.D.
Professor

Research Interests:
Cholesterol, high density lipoprotein (HDL), caveolae, signaling, lipid-binding, atherosclerosis, cholesterol-binding proteins, plasma membrane

Summary:
The research in our laboratory deals with the formation, activity and turnover of high density lipoprotein (HDL), the 'good cholesterol' component of plasma lipoproteins. HDL lowers peripheral cell cholesterol levels by promoting cholesterol transport to the liver. It regulates signaling across cell membranes by controlling the cholesterol content of lipid rafts and caveolae, cell surface complexes of signaling proteins. Finally, HDL opposes inflammation when it acts as a scaffold for enzymes that bind and break down oxidized lipids to harmless by-products. Low HDL is a strong indicator of increased risk for human atherosclerotic heart disease. The development of HDL-raising drugs has recently accelerated. Our ability to raise plasma HDL levels will depend on defining the molecular mechanisms by which HDL is formed and recycled.

CVRIHead