2015
DOI: 10.1194/jlr.c061366
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SAA: a link between cholesterol efflux capacity and inflammation?

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Cited by 15 publications
(18 citation statements)
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“…Low HDL cholesterol concentration in active sarcoidosis may result from elevated serum amyloid A (SAA) concentration [27], which can displace apo A-I from HDL exposing the lipoprotein particle to rapid clearance. Recently, studies of HDL proteome have raised the possibility of a link between SAA, cholesterol efflux capacity, inflammation and atherosclerosis [28].…”
Section: Discussionmentioning
confidence: 99%
“…Low HDL cholesterol concentration in active sarcoidosis may result from elevated serum amyloid A (SAA) concentration [27], which can displace apo A-I from HDL exposing the lipoprotein particle to rapid clearance. Recently, studies of HDL proteome have raised the possibility of a link between SAA, cholesterol efflux capacity, inflammation and atherosclerosis [28].…”
Section: Discussionmentioning
confidence: 99%
“…Treatment of wild-type mice with silver nitrate induced an acute phase response and markedly remodelled the HDL proteome of the wild-type mice, but not that of the mice null for SAA1 and SAA2. 13 , 14 HDL obtained from the wild-type mice after silver nitrate treatment showed a marked decrease in its ability to promote cholesterol efflux from macrophages that was inversely correlated with the SAA content of the HDL. 13 , 14 In contrast, HDL obtained after silver nitrate treatment from the mice null for Saa1/2 retained its ability to promote cholesterol efflux.…”
mentioning
confidence: 94%
“…The ability of HDL from the endotoxin-treated subjects to accept cholesterol from macrophages was inversely correlated with the content of SAA1/2 in the HDL. 13 , 14 While the composition and function of HDL from the endotoxin-treated subjects was significantly changed, the lipid composition of HDL and the plasma levels of HDL cholesterol, LDL cholesterol and triglycerides did not change. 13 , 14 In mouse studies, in the absence of inflammation, the protein composition of HDL from wild-type mice was virtually identical to that of HDL from mice null for Saa1/2 and hence lacking SAA1 and SAA2.…”
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confidence: 98%
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