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ABSTRACT: Objective
The c-Jun N-terminal kinase (JNK) family regulates fundamental physiological processes including apoptosis and metabolism. Although JNK2 is known to promote foam cell formation during atherosclerosis, the potential role of JNK1 is uncertain. We examined the potential influence of JNK1 and its negative regulator, MAP kinase phosphatase-1 (MKP-1), on endothelial cell (EC) injury and early lesion formation using hypercholesterolemic LDLR(-/-) mice.Methods and results
To assess the function of JNK1 in early atherogenesis, we measured EC apoptosis and lesion formation in LDLR(-/-) or LDLR(-/-)/JNK1(-/-) mice exposed to a high fat diet for 6 weeks. En face staining using antibodies that recognise active, cleaved caspase-3 (apoptosis) or using Sudan IV (lipid deposition)
SUBMITTER: Amini N
PROVIDER: S-EPMC4104040 | biostudies-literature | 2014 Aug
REPOSITORIES: biostudies-literature