Journal
SCIENCE
Volume 306, Issue 5701, Pages 1558-1561Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1101909
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In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE(-/-) mice simultaneously lacking JNK2 (ApoE(-/-) JNK2(-/-) mice), but not ApoE(-/-) JNK1(-/-) mice, developed less atherosclerosis than do ApoE(-/-) mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis.
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