Abstract:
:Reverse cholesterol transport (RCT) is an antiatherogenic process in which excessive cholesterol from peripheral tissues is transported to the liver and finally excreted from the body via the bile. The nuclear receptor liver receptor homolog 1 (LRH-1) drives expression of genes regulating RCT, and its activity can be modified by different posttranslational modifications. Here, we show that atherosclerosis-prone mice carrying a mutation that abolishes SUMOylation of LRH-1 on K289R develop less aortic plaques than control littermates when exposed to a high-cholesterol diet. The mechanism underlying this atheroprotection involves an increase in RCT and its associated hepatic genes and is secondary to a compromised interaction of LRH-1 K289R with the corepressor prospero homeobox protein 1 (PROX1). Our study reveals that the SUMOylation status of a single nuclear receptor lysine residue can impact the development of a complex metabolic disease such as atherosclerosis.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Stein S,Oosterveer MH,Mataki C,Xu P,Lemos V,Havinga R,Dittner C,Ryu D,Menzies KJ,Wang X,Perino A,Houten SM,Melchior F,Schoonjans Kdoi
10.1016/j.cmet.2014.07.023subject
Has Abstractpub_date
2014-10-07 00:00:00pages
603-13issue
4eissn
1550-4131issn
1932-7420pii
S1550-4131(14)00331-3journal_volume
20pub_type
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