Portrait of Moritz and Helene Leffmann Portraits Couples

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Portrait of unidentified woman Portraits Women

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Portrait of unidentified man Portraits Men

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Autographed portrait of Dr. Bernhard Bardach Portraits Men

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Portrait of Hugo Pollak with wife Thekla Lichtenstadt Pollak and their children Hans Pollak and Zdenka (Mimi) Pollak seated outdoors Portraits Family

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Cellular Cholesterol Accumulation and Egress from Endosomal Compartments

One of the most important factors determining the development of atherosclerosis is the amount of LDL particles in the circulation. In general, LDL particles are clinically regarded as “bad cholesterol” since these particles get entrapped within the vascular wall, leading to atherosclerosis. Circulating HDL particles are conversely regarded as “good cholesterol” because of their ability to transport cholesterol from peripheral tissues to the liver for secretion as bile salts. Once inside the artery wall LDL particles are engulfed by macrophages, resulting in macrophage foam cells. If the macrophage foam cells are not able to efflux the cholesterol back into the bloodstream, the excessive cholesterol ultimately leads to cell death, and the deposition of cellular debris within the atherosclerotic lesion. The cells ability to secrete cholesterol is mainly dependent on the ABCA1 transporter (ATP-binding cassette transporter A1) which transfers cellular cholesterol to extracellular apoA-I (apolipoprotein A-I) particles, leading to the generation of nascent HDL particles. The process of atherosclerotic plaque development is therefore to a large extent a cellular one, in which the capacity of the macrophages in handling the excessive cholesterol load determines the progression of lesion development. In this work we have studied the cellular mechanisms that regulate the trafficking of LDL-derived cholesterol from endosomal compartments to other parts of the cell. As a basis for the study we have utilized cells from patients with Niemann-Pick type C disease, a genetic disorder resulting from mutations in the NPC1 and NPC2 genes. In these cells, cholesterol is entrapped within the endosomal compartment, and is not available for efflux. By identifying proteins that bypass the cholesterol trafficking defect, we were able to identify the small GTPase Rab8 as an important protein involved in ABCA1 dependent cholesterol efflux. In the study, we show that Rab8 regulates cholesterol efflux in human macrophages by facilitating intracellular cholesterol transport, as well as by regulating the plasma membrane availability of ABCA1. Collectively, these results give new insight in to atherosclerotic lesion development and intracellular cholesterol processing.

Portrait of Elizabeth Sofer Portraits Women

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Portrait of Frieda Michaelis; Munich Portraits Women

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New Year's greetings postcard with portrait of Sigmund and Toni Feist with two unidentified boys (perhaps students at Feist's private school in Mainz) Portraits; Groups

Printed: Prosit Neujahr!; Handwritten dedication

Portrait of Ludwig Feist (far left) perhaps with Toni and Sigmund Feist Portraits; Groups

Handwritten caption: Aufgenommen am 9. VIII. 1908 vor der Stadthalle in Mainz. Letztes Bild meines Bruders Ludwig Feist (gest. 2. XI. 08)

Professor Lichtenberger, German literature professor at the Sorbonne, with Toni and Sigmund Feist Portraits; Groups

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Portrait of Dr. S. Theodor Stein; Frankfurt am Main Portraits Men

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Portrait of unidentified man wearing medals and holding rifle, standing in front of shooting target Portraits Men

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