• No results found

Cholesterol and phospholipid transporters in atherosclerotic lesion development

N/A
N/A
Protected

Academic year: 2021

Share "Cholesterol and phospholipid transporters in atherosclerotic lesion development"

Copied!
7
0
0

Bezig met laden.... (Bekijk nu de volledige tekst)

Hele tekst

(1)

Cholesterol and phospholipid transporters in atherosclerotic lesion development

Pennings, M.

Citation

Pennings, M. (2008, September 16). Cholesterol and phospholipid transporters in

atherosclerotic lesion development. Division of Biopharmaceutics of the Leiden/Amsterdam Center for Drug Research|Leiden University Medical Center (LUMC), Leiden University.

Retrieved from https://hdl.handle.net/1887/13099

Version: Corrected Publisher’s Version

License: Licence agreement concerning inclusion of doctoral thesis in the Institutional Repository of the University of Leiden

Downloaded from: https://hdl.handle.net/1887/13099

Note: To cite this publication please use the final published version (if applicable).

(2)

Cholesterol and Phospholipid Transporters in Atherosclerotic Lesion Development

Proefschrift

ter verkrijging van

de graad van Doctor aan de Universiteit van Leiden, op gezag van de Rector Magnificus prof.mr. P.F. van der Heijden,

volgens besluit van het College voor Promoties te verdedigen op 16 september 2008

klokke 13:45 uur

door

Marieke Pennings geboren te Zaanstad

in 1976

(3)

Promotiecommissie

Promotor : Prof. Dr. Th.J.C. Van Berkel

Co-promotor : Dr. M. Van Eck

Referent : Prof. Dr. Ir. L.M. Havekes

Overige leden : Prof. Dr. M. Danhof

Dr. A.K. Groen (UvA) Prof. Dr. E.R. de Kloet Prof. Dr. F. Kuipers (RUG)

The study described in this thesis was financially supported by a ZonMw grant (192-02-063) and was performed at the Division of Biopharmaceutics of the Leiden Amsterdam Center for Drug Research, the Netherlands.

- 2 -

(4)
(5)

- 4 -

(6)

Contents

Chapter 1 Introduction 7

Chapter 2 Regulation of cholesterol homeostasis in macrophages 19 and consequences for atherosclerotic lesion development

Chapter 3 Bone marrow derived multidrug resistance protein ABCB4 39 protects against atherosclerotic lesion development in LDL

receptor knock out mice

Chapter 4 Scavenger receptor BI and ATP-binding cassette transporter A1 59 in reverse cholesterol transport and atherosclerosis

Chapter 5 ABCA1/SR-BI double deficient mice demonstrate the 79 independent roles for ABCA1 and SR-BI in reverse

cholesterol transport

Chapter 6 Massive foam cell formation, atherosclerotic lesion development, 95 and inflammation by combined deletion of ABCA1 and SR-BI in

bone marrow-derived cells in LDL receptor knockout mice

Chapter 7 Summary and concluding remarks 119

Nederlandse Samenvatting 125

Abbreviations 133

Publications 135

Curriculum Vitae 137

(7)

- 6 -

Referenties

GERELATEERDE DOCUMENTEN

Mdr1 Multidrug resistance protein 1 Mdr2 Multidrug resistance protein 2 SR-BI Scavenger receptor class B type I RCT Reverse Cholesterol transport VLDL Very

Massive foam cell formation, atherosclerotic lesion development, and inflammation by combined deletion of ABCA1 and SR-BI in bone marrow-derived cells in LDL receptor knockout

Division of Biopharmaceutics of the Leiden/Amsterdam Center for Drug Research|Leiden University Medical Center (LUMC), Leiden University.. Retrieved

Het gemis van ABCA1 en SR-BI op macrofagen kan niet volledig gecompenseerd worden door andere cholesterol transporterende eiwitten.

(A) Cell cycle analysis in RAW 264.7 macrophages in control (white) and MIC-1 treated cells (grey) in combination with TGFβRII blockade (black) (B) Cellular proliferation as

Representative MoMa-2 slides for controls (centre panel) and GRK2 +/- chimeras (right panel), macrophages are depicted in blue. Images 50x magniication. A) Collagen deposition

Figure 1: Induction of chronic Graft versus Host Disease in CCR7 -/- chimeras.A) Total number of bone marrow cells from WT controls (black) and CCR7 -/- chimeras (white).

Taken together our data clearly establish a causal role for neutrophils in the development of atherosclerosis Furthermore we hypothesize that under conditions of