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I demonstrated that the C-terminal domain of apoA-I participates in ABCA1-mediated lipid efflux (2002) and provided the first evidence for the essential contribution of hepatic ABCA1 to the lipidation of nascent HDL as well as exogenous apoA-I (Kiss, 2003). Wth J. Cohen and R. McPherson, we showed that multiple non-synonymous mutations in ABCA1 contribute to the low HDL phenotype (2004). Pursuing this work with R. McPherson (2005), we showed that efflux defects are frequent in low HDL syndrome and genetically heterogeneous. Furthermore, the monocyte-derived macrophages of these patients present with a pro-inflammatory phenotype that is independent of cholesterol efflux (Kiss, 2007; Sarov-Blat, 2007). This indicates that differentiation of monocytes under condition of low HDL leads to the selection of inflammatory monocytes, a new parameter of the anti-inflammatory properties of HDL.
In macrophages I showed that SR-A and LDL receptor transport cholesterol through distinct pathways (Wang, 2006) and that efflux through HDL is significant contributor to reverse cholesterol transport (Wang, 2007). With R.S. Kiss (2005), I showed that GULP is an adaptor to LRP that controls the traffic of cholesterol to and out of the late endosomes through its effects on prosaposin and sphingolipid transport. Recently, I discovered that cathepsin D is a positive regulator of ABCA1 (Haidar, 2006) and demonstrated that NPC1 activity activates CTSD and subsequently ABCA1 in hepatocytes but not macrophages (Wang, 2007). We were also the first to demonstrate that reverse cholesterol transport from macrophages that do not express ABCA1 is impaired (Wang, 2007).
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Mireille Ouimet,Stefan Koster, Erik Sakowski,Bhama Ramkhelawon,Coen van Solingen,Scott Oldebeken,Denuja Karunakaran,Cynthia Portal-Celhay,Frederick J Sheedy, Tathagat Dutta Ray,Katharine Cecchini, Philip D Zamore,
NATURE IMMUNOLOGYno. 6 (2016): 677-686
Journal of nuclear medicine : official publication, Society of Nuclear Medicineno. 11 (2016): 1784-1791
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