136 - Apolipoprotein J ablation triggers atherosclerosis in a chow diet-fed LDLR-KO mice (ID 415)
Abstract
Background and Aims
Apolipoprotein J (apoJ) is an extracellular chaperone involved in the clearance of misfolded proteins, which is partly transported in blood bound to lipoproteins and is highly expressed in atherosclerotic arteries. However, the role of apoJ in atherogenesis is unclear. This study analyzes the effect of the genetic ablation of apoJ in LDL receptor knockout (LDLR-KO) mice.
Methods
We studied wild-type (WT), LDLR-KO, apoJ-KO and double KO apoJ-LDLR (D-KO) male mice fed with chow diet (CD) or western-type diet (WD). Mice were sacrificed after eight weeks and the aortic arch was analyzed for the presence of atherosclerotic lesions. Lipid profile, composition and particle size of isolated VLDL, LDL and HDL were analyzed.
Results
Neither WT nor apoJ-KO mice developed hyperlipemia and atherosclerotic lesions either on CD or WD. LDLR-KO mice presented hyperlipemia and large atherosclerotic lesions on WD, whereas the size of these lesions on CD was 15-fold smaller. D-KO mice fed with WD developed atherosclerotic lesions at a similar extent as LDLR-KO on WD. Surprisingly, despite that D-KO on CD presented moderate hyperlipemia, these mice developed extensive lesions 10-fold larger than LDLR-KO fed with CD. No difference in the size or composition of lipoprotein particles was observed between LDLR-KO and D-KO either on WD or CD.
Conclusions
Generally, the development of atherosclerosis in LDLR-KO mice requires very high lipid levels in blood, but in D-KO mice lesions appeared with only moderately increased lipids. Our results demonstrate that the lack of apoJ promotes the development of atherosclerotic lesions in a context of moderate hyperlipemia.
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